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2
PHYSIOLOGY OF SPORT AND
EXERCISE
SEVENTH EDITION
W. Larry Kenney, PhD
Pennsylvania State University, University Park
Jack H. Wilmore, PhD
University of Texas, Austin
David L. Costill, PhD
Ball State University, Muncie, Indiana
3
Library of Congress Cataloging-in-Publication Data
Names: Kenney, W. Larry, author. | Wilmore, Jack H., 1938-2014, author. | Costill,
David L., author.
Title: Physiology of sport and exercise / W. Larry Kenney, Jack H. Wilmore, David
L. Costill.
Description: Seventh edition. | Champaign, IL : Human Kinetics, [2020] | Includes
bibliographical references and index.
Identifiers: LCCN 2018040753 (print) | LCCN 2018041421 (ebook) | ISBN
9781492574859 (epub) | ISBN 9781492589198 (PDF) | ISBN 9781492572299
(hardback)
Subjects: | MESH: Sports--physiology | Exercise--physiology | Physical Fitness-physiology | Physical Endurance--physiology
Classification: LCC QP301 (ebook) | LCC QP301 (print) | NLM QT 260 | DDC
612/.044--dc23
LC record available at https://lccn.loc.gov/2018040753
ISBN: 978-1-4925-7229-9 (hardback)
ISBN: 978-1-4925-7486-6 (loose-leaf)
Copyright © 2020 by W. Larry Kenney and David L. Costill
Copyright © 2015, 2012 by W. Larry Kenney, Jack H. Wilmore, and David L. Costill
Copyright © 2008 by Jack H. Wilmore, David L. Costill, and W. Larry Kenney
Copyright © 2004, 1999, 1994 by Jack H. Wilmore and David L. Costill
All rights reserved. Except for use in a review, the reproduction or utilization of this
work in any form or by any electronic, mechanical, or other means, now known or
hereafter invented, including xerography, photocopying, and recording, and in any
information storage and retrieval system, is forbidden without the written
permission of the publisher.
Permission notices for material reprinted in this book from other sources can be
found on page xix.
The web addresses cited in this text were current as of January 2019, unless
otherwise noted.
Senior Acquisitions Editor: Amy N. Tocco; Developmental Editor: Judy Park;
Managing Editor: Anna Lan Seaman; Copyeditor: Joy Hoppenot; Indexer:
Alisha Jeddeloh; Permissions Manager: Dalene Reeder; Senior Graphic
Designer: Nancy Rasmus; Cover Designer: Keri Evans; Cover Design
4
Associate: Susan Rothermel Allen; Photograph (cover): AMR Image/Getty
Images; Photo Asset Manager: Laura Fitch; Visual Production Assistant:
Joyce Brumfield; Photo Production Manager: Jason Allen; Senior Art Manager:
Kelly Hendren; Illustrations: © Human Kinetics, unless otherwise noted; Printer:
Walsworth
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E7426 (hardback)/E7449 (loose-leaf)
5
was an exceptional teacher, researcher, writer, and
lecturer. His ability to communicate the complexities of exercise
physiology to students, health professionals, and the general public
is evident in this textbook. As the lead author of the first four editions
of Physiology of Sport and Exercise, Jack took great pride in the
clarity and accuracy of its contents. This book was his brainchild.
Jack began his career in exercise physiology at Ithaca College in
New York. He then held professorships at the University of California
at Berkley, University of California at Davis, University of Arizona,
University of Texas, and Texas A&M. He published more than 300
scientific and lay articles, 15 books, and 55 chapters in other texts. In
addition to serving as president of the American College of Sports
Medicine (ACSM) and the American Academy of Kinesiology and
Physical Education, Jack was active in many other professional
organizations. His star status in sports medicine was rewarded with
a long list of honors including the Citation and Honor Awards from
ACSM. The achievements in his 50-year career are the basis for our
current knowledge of the critical importance of regular physical
Jack H. Wilmore
6
activity in health, disease, and aging. His impact on students and the
general public was the envy of all his colleagues. Physiology of Sport
and Exercise lives on as a legacy of an exceptional scientist in sport
and exercise and friend to many. He is missed by family, friends, and
colleagues alike, and this book remains an enduring part of his
legacy.
7
Contents
Research Perspectives Finder
Preface
Student and Instructor Resources
Acknowledgments
Photo Credits
INTRODUCTION:
An Introduction to Exercise and Sport
Physiology
Focus of Exercise and Sport Physiology
Acute and Chronic Responses to Exercise
The Evolution of Exercise Physiology
Exercise Physiology in the 21st Century
Research: The Foundation for Understanding
PART I Exercising Muscle
1
Structure and Function of Exercising Muscle
Anatomy of Skeletal Muscle
Muscle Fiber Contraction
Muscle Fiber Types
Skeletal Muscle and Exercise
2
Fuel for Exercise: Bioenergetics and Muscle
Metabolism
Energy Substrates
Controlling the Rate of Energy Production
Storing Energy: High-Energy Phosphates
8
The Basic Energy Systems
Interaction of the Energy Systems
The Crossover Concept
The Oxidative Capacity of Muscle
3
Neural Control of Exercising Muscle
Structure and Function of the Nervous System
Central Nervous System
Peripheral Nervous System
Sensory-Motor Integration
4
Hormonal Control During Exercise
The Endocrine System
Endocrine Glands and Their Hormones: An Overview
Hormonal Regulation of Metabolism During Exercise
Hormonal Regulation of Fluid and Electrolytes During Exercise
Hormonal Regulation of Caloric Intake
5
Energy Expenditure, Fatigue, and Muscle
Soreness
Measuring Energy Expenditure
Energy Expenditure at Rest and During Exercise
Fatigue and Its Causes
Critical Power: The Link Between Energy Expenditure and Fatigue
Muscle Soreness and Muscle Cramps
PART II Cardiovascular and Respiratory
Function
6
The Cardiovascular System and Its Control
The Heart
Vascular System
Blood
9
7
The Respiratory System and Its Regulation
Pulmonary Ventilation
Pulmonary Volumes
Pulmonary Diffusion
Transport of Oxygen and Carbon Dioxide in the Blood
Gas Exchange at the Muscles
Regulation of Pulmonary Ventilation
Afferent Feedback From Exercising Limbs
8
Cardiorespiratory Responses to Acute
Exercise
Cardiovascular Responses to Acute Exercise
Respiratory Responses to Acute Exercise
PART III Exercise Training
9
Principles of Exercise Training
Terminology
General Principles of Training
Resistance Training Programs
Anaerobic and Aerobic Power Training Programs
10
Adaptations to Resistance Training
Resistance Training and Gains in Muscular Fitness
Mechanisms of Gains in Muscle Strength
Interaction Between Resistance Training and Diet
Resistance Training for Special Populations
11
Adaptations to Aerobic and Anaerobic
Training
Adaptations to Aerobic Training
Adaptations to Anaerobic Training
Adaptations to High-Intensity Interval Training
Specificity of Training and Cross-Training
10
PART IV Environmental Influences on
Performance
12
Exercise in Hot and Cold Environments
Body Temperature Regulation
Physiological Responses to Exercise in the Heat
Health Risks During Exercise in the Heat
Acclimation to Exercise in the Heat
Exercise in the Cold
Physiological Responses to Exercise in the Cold
Health Risks During Exercise in the Cold
13
Exercise at Altitude
Environmental Conditions at Altitude
Physiological Responses to Acute Altitude Exposure
Exercise and Sport Performance at Altitude
Acclimation: Chronic Exposure to Altitude
Altitude: Optimizing Training and Performance
Health Risks of Acute Exposure to Altitude
PART V Optimizing Performance in Sport
14
Training for Sport
Optimizing Training
Periodization of Training
Overtraining
Tapering for Peak Performance
Detraining
15
Body Composition and Nutrition for Sport
Assessing Body Composition
Body Composition, Weight, and Sport Performance
Classification of Nutrients
Water and Electrolyte Balance
11
Nutrition and Athletic Performance
16
Ergogenic Aids in Sport
Researching Ergogenic Aids
Ergogenic Nutrition Aids
Anti-Doping Codes and Drug Testing
Prohibited Substances and Techniques
PART VI Age and Sex Considerations in Sport
and Exercise
17
Children and Adolescents in Sport and
Exercise
Growth, Development, and Maturation
Physiological Responses to Acute Exercise
Physiological Adaptations to Exercise Training
Physical Activity Patterns Among Youth
Sport Performance and Specialization
Special Issues
18
Aging in Sport and Exercise
Height, Weight, and Body Composition
Physiological Responses to Acute Exercise
Physiological Adaptations to Exercise Training
Sport Performance
Special Issues
19
Sex Differences in Sport and Exercise
Sex Versus Gender in Exercise Physiology
Body Size and Composition
Physiological Responses to Acute Exercise
Physiological Adaptations to Exercise Training
Sport Performance
Special Issues
12
PART VII Physical Activity for Health and
Fitness
20
Prescription of Exercise for Health and
Fitness
Health Benefits of Regular Physical Activity and Exercise
Physical Activity Recommendations
Health Screening
Exercise Prescription
Monitoring Exercise Intensity
Exercise Programming
Exercise and Rehabilitation of People with Diseases
21
Cardiovascular Disease and Physical
Activity
Prevalence of Cardiovascular Disease
Forms of Cardiovascular Disease
Understanding the Disease Process
Cardiovascular Disease Risk
Reducing Risk Through Physical Activity
Risk of Heart Attack and Death During Exercise
Exercise Training and Rehabilitation of Patients with Heart Disease
22
Obesity, Diabetes, and Physical Activity
Understanding Obesity
Weight Loss
Management Guidelines for Overweight and Obesity
Role of Physical Activity in Weight Management and Risk Reduction
Understanding Diabetes
Treatment of Diabetes
Role of Physical Activity in Diabetes
Glossary
References
Index
13
About the Authors
14
Research Perspectives Finder
1.1
1.2
1.3
2.1
2.2
2.3
3.1
3.2
3.3
3.4
4.1
4.2
4.3
5.1
5.2
5.3
5.4
6.1
6.2
6.3
7.1
7.2
7.3
7.4
8.1
8.2
8.3
9.1
9.2
9.3
Muscle Changes After Only 6 Weeks of Training
Curving Muscle Fascicles
More About Titin
White, Brown, and (Perhaps) Beige Fat in Humans
Lifelong Training Can Lead to More Efficient Fuel Utilization
Does the Muscle Fiber’s Oxidative Capacity Determine Fitness Level?
Motor Units Adapt to High-Intensity Interval Training
Aging Reduces Rapid Strength
Sex Differences in Skeletal Muscle Fiber Types
Nontraditional Factors That Impair Neuromuscular Control
Does Having More Testosterone Give You a Competitive Advantage?
Endurance Training for More Red Blood Cells
Does Environmental Temperature Alter the Hormones That Control Appetite?
Energy Expenditure of Walking
Can You Talk Yourself Out of Fatiguing?
Are Muscle Fatigue and Exercise Inefficiency the Same Thing?
Delayed-Onset Muscle Soreness May Be Different in Men and Women
The Debate Surrounding Exercise Training– Induced Reductions in Heart Rate
Can Too Much Exercise Be Bad for Your Heart?
Vascular Adaptations to Exercise Training in Postmenopausal Women
Sprint Interval Training for Respiratory Muscles
Exercise Training Offsets Decreases in Lung Diffusing Capacity with Aging
Ventilation During Exercise in Asthma
Regular Exercise Reduces Respiratory Disease Mortality
HUNTing for a Better Prediction of Maximal Heart Rate
Is Recovery a Distinct Cardiovascular State?
Posture Affects Ventilation During Recovery After Exercise
Can Aerobic Exercise Increase Muscle Size?
Tabata Training: The Original HIIT
Exploring the Mechanisms That Increase
O2max with HIIT
10.1 Aerobic Benefits From Resistance Exercise Training
10.2 Lifting Before Bedtime for Enhanced Muscle Protein Synthesis
10.3 Resistance Training Can Improve Health Without Changing BMI
11.1
How Much Can
O2max Improve?
11.2 Brief, Intense Stair Climbing
11.3 Do Ice Baths Increase Recovery and Endurance Performance?
11.4 Age and Responses to HIIT
12.1 Dehydration Challenges the Cardiovascular System During Exercise in the Heat
12.2 Tattoos and Sweating
12.3 Fuel for Shivering
12.4 The Yukon Arctic Ultramarathon
13.1 Human Adaptation to High Altitude: Tibetan and Sherpa Physiology
13.2 Altitude Training for Swimmers
13.3 Should Athletes Live Extra High and Train Low?
14.1 Periodization of High-Intensity Training Models and Endurance Adaptation
15
14.2
14.3
15.1
15.2
15.3
15.4
16.1
16.2
16.3
16.4
17.1
17.2
17.3
18.1
18.2
18.3
19.1
19.2
19.3
19.4
20.1
20.2
20.3
20.4
21.1
21.2
21.3
22.1
22.2
22.3
Peak Performance During the Taper Phase
Disturbed Sleep and Increased Illness in Overreached Athletes
Exercise Type and Body Composition
Meal Timing and the Aerobic Exercise Window
Low-Carb and Low-Fat Diets
The Myth of High-Protein Diets
The “Nocebo” Effect on Sport Performance
Analgesic Use in Sport
Caffeine Use in Cycling
Creatine Supplementation Plus Resistance Exercise to Prevent Sarcopenia
Cognitive Benefits of Exercise for Children
Physical Activity and Obesity in Children Around the World
Declines in Physical Activity During Adolescence
Centenarian Athletes
Physical Activity and Cognitive Function in Older Adults
Age-Related Changes in Human Skeletal Muscle
Do Men Lose More Weight Than Women with Regular Exercise?
Men Are More Likely Than Women to Slow Down During a Marathon
Should Female Athletes Be Tested for Iron Deficiency and Anemia?
Land Versus Water Exercise in Pregnancy
Sitting, Physical Activity, and Mortality
Revised Physical Activity Guidelines for Americans
Exercise and the Brain
Golf Is (Probably) Good for Your Health
Long-Term Marathon Running Reduces Coronary Artery Plaque Formation in Women
Maintaining Fitness Into Middle Age Reduces CVD Risk
Physical Activity Reduces Cigarette Cravings
The Fat-but-Fit Paradox
Sedentary Behavior, Physical Activity, and Adiposity
Metformin or Exercise or Both to Treat Diabetes?
16
Preface
Physiology is the study of how the human body functions. Cells,
tissues, organs, and systems intricately and precisely communicate
and integrate to coordinate the body’s myriad physiological
functions. Even at rest, the body is physiologically quite active.
Imagine, then, how much more active all of these body systems
become when you engage in exercise. During exercise, nerves
excite muscles to contract. Exercising muscles are metabolically
active and require more nutrients, more oxygen, and efficient
clearance of waste products. The autonomic nervous system and
endocrine glands combine to fine-tune these processes. How does
the whole body respond to the increased physiological demands of
physical activity in all its forms?
That is the key question when you study the physiology of sport
and exercise. Physiology of Sport and Exercise, Seventh Edition,
introduces you to the fields of sport and exercise physiology. Our
goal is to build on the knowledge that you developed during basic
coursework in human anatomy and physiology and to apply those
principles in studying how the body (1) performs and responds to the
added demands of an acute bout of exercise and (2) adapts to
repeated bouts of exercise (i.e., exercise training).
What’s New in the Seventh Edition
The seventh edition of Physiology of Sport and Exercise maintains
the previous edition’s high standard for illustrations, photos, and
medical artwork. This visual detail, clarity, and realism allow both a
greater insight into the physiological responses to exercise and a
better understanding of the underlying research. In addition, the text
is now augmented with animations, audio clips, and video clips,
provided online in the student web study guide and separately for
instructors. Throughout the text, you will find icons to identify pieces
17
of artwork that are the basis for an animation or that have an
accompanying audio clip. Accessing these resources will further aid
understanding of the illustrations and the physiological processes
they represent. In addition, video clips feature experts in the field
discussing exciting current topics of research.
The new edition also brings back the Research Perspective
elements introduced in the last edition that highlight interesting
current research. These inserts discuss a wide range of important
new or developing topics in sport and exercise physiology, providing
interested students with additional insight into the state of research
in the field. We have also revised the introductory chapter to include
information on new frontiers in exercise physiology in the 21st
century such as genomics and epigenetics, chapter 5 to include
more detailed coverage of mechanisms associated with fatigue and
muscle cramps, chapter 11 to expand coverage of high-intensity
interval training, and chapter 17 to focus more on health benefits of
physical activity in children and adolescents. In addition, we have
extensively updated the text to include the latest research on
important topics in the field, including the following:
New information on length–tension and force–velocity
relations in muscle (chapter 1) and individual variability in
appetite hormones (chapter 4)
Newly added sections on the crossover concept (chapter 2),
critical power (chapter 5), functional sympatholysis (chapter
6), the oxygen cascade (chapters 7 and 13), group exercise
(chapter 9), and exercise and mobility in aging (chapter 18)
Updated information on the role of maximal stroke volume in
determining maximal aerobic capacity (chapter 8)
Expanded mechanistic discussion of protein synthesis in
muscle hypertrophy (chapter 10)
Revision of information to reflect published guidelines by
professional organizations on nutrition and athletic
performance (chapter 15), exercise and pregnancy (chapter
19), and health-related screening, fitness testing, and
exercise prescription (chapter 20)
18
All of these changes were made while retaining our emphasis on
the ease of reading and understanding that have made this book the
leading text for introducing students to this exciting field. The overall
structure and progression of the text have been retained from the
sixth edition. Our first focus is on muscle and how its needs are
altered as an individual goes from a resting to an active state and
how these needs are supported by—and interact with—other body
systems. In later chapters we address principles of exercise training;
considerations of environmental factors of heat, cold, and altitude;
sport performance; and exercise for disease prevention.
Organization of the Seventh Edition
We begin in the introduction with a historical overview of sport and
exercise physiology as they have emerged from the parent
disciplines of anatomy and physiology, and we explain basic
concepts that are used throughout the text. In parts I and II, we
review the major physiological systems, focusing on their responses
to acute bouts of exercise. In part I, we examine how the muscular,
metabolic, nervous, and endocrine systems interact to produce body
movement. In part II, we look at how the cardiovascular and
respiratory systems continue to deliver nutrients and oxygen to the
active muscles and transport waste products away during physical
activity. In part III, we consider how these systems adapt to chronic
exposure to exercise (i.e., training).
We change perspective in part IV to examine the impact of the
external environment on physical performance. We consider the
body’s response to heat and cold, and then we examine the impact
of low atmospheric pressure experienced at altitude. In part V, we
shift attention to how athletes can optimize physical performance.
We evaluate the effects of different types and volumes of training.
We consider the importance of appropriate body composition for
optimal performance and examine athletes’ special dietary needs, as
well as how nutrition can be used to enhance performance. Finally,
we explore the use of ergogenic aids—substances purported to
improve athletic ability.
In part VI, we examine unique considerations for specific
populations. We look first at the processes of growth and
19
development and how they affect the performance capabilities of
young athletes. We evaluate changes that occur in physical
performance as people age and explore the ways in which physical
activity can help maintain health and independence. Finally, we
examine issues and special physiological concerns of female
athletes.
In the final part of the book, part VII, we turn our attention to the
application of sport and exercise physiology to prevent and treat
various diseases and the use of exercise for rehabilitation. We look
at prescribing exercise for maintaining health and fitness, and we
then close the book with a discussion of cardiovascular disease,
obesity, and diabetes.
Special Features in the Seventh Edition
This seventh edition of Physiology of Sport and Exercise is designed
with the goal of making learning easy and enjoyable. This text is
comprehensive, but the many special features included will help you
progress through the book without being overwhelmed by its scope.
In addition to these features, the fully updated web study guide that
accompanies this text provides opportunities for interactive learning
and review, along with animations, audio clips, and video clips to
enhance your understanding of the text.
Each chapter in the book begins with a chapter outline with page
numbers to help you locate material. Also noted in the chapter
20
outline are the web study guide activities relating to each section of
the chapter. Each chapter begins with a brief story that explores a
real-world application of the concepts presented.
Within each chapter, the Research Perspective elements
introduce you to important topics in current exercise physiology
research. You will also find icons to alert you to animations and audio
clips that will help you understand important figures and to video
clips that provide expanded discussion on current topics in the field:
Animation icons identify figures that are also provided as
animations.
Audio icons identify figures that are further explained in an
accompanying audio clip.
Video icons let you know when a video clip on a topic is
available.
As you read through, you will also find In Review elements that
summarize the major points presented in the previous sections. And
at the end of the chapter, the In Closing wraps things up and notes
how what you have learned sets the stage for the topics to come.
21
22
Key terms are in bold in the text, listed at the end of each chapter,
and defined in the glossary at the end of the book. At each chapter’s
end, you will also find study questions to test your knowledge of the
chapter’s contents and a reminder of the study guide activities that
are available, along with the web address of the online study guide.
At the end of the book is a comprehensive glossary that includes
definitions of all key terms, a listing of numbered references for the
sources cited in each chapter, and a thorough index. Finally, printed
on the inside front and back covers for easy reference are lists of
common abbreviations and conversions.
Instructors using this text in their courses will find a wealth of
updated
ancillary
materials
available
at
23
www.HumanKinetics.com/PhysiologyOf SportAndExercise, including
an instructor guide, a presentation package, a test package, chapter
quizzes, and an image bank. The instructor ancillaries also include
convenient access to the animations, video clips, and audio clips.
You might read this book only because it is a required text for a
course. But we hope that the information will entice you to continue
to study this relatively new and exciting area. We hope at the very
least to further your interest in and understanding of your body’s
marvelous abilities to perform various types and intensities of
exercise and sports, to adapt to stressful situations, and to improve
its physiological capacities. This book is useful not only for anyone
who pursues a career in exercise or sport science but also for
anyone who wants to be active, healthy, and fit.
24
25
26
Student and Instructor Resources
Student Resources
Students,
visit
the
free
web
study
guide
at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
for
interactive learning activities—all of which can be conducted outside
the lab or classroom—as well as animations, video clips, and audio
clips to aid your learning. You’ll be able to apply key concepts by
conducting experiments and recording your own physiological
responses to exercise. The guide includes activities and quizzes that
test your knowledge of the material as you prepare for classroom
quizzes or tests. You’ll also have access to links to professional
journals and information on organizations and careers in the field.
Updated for the seventh edition, the web study guide includes the
following multimedia content:
26 animated versions of artwork from the text that will help you to
understand physiological processes
27 video discussions with experts in the field of exercise
physiology
66 audio clips that describe the processes shown in figures
Look for the icons in the text to know when this additional content is
available. As you work to understand a concept illustrated in a figure,
refer to the audio or animation for an explanation and to build your
understanding. In combination with the web study guide activities,
the animations, video, and audio allow you to practice, review, and
develop knowledge and skills about the physiology of sport and
exercise.
Instructor Resources
Instructor Guide
27
Specifically developed for instructors who have adopted Physiology
of Sport and Exercise, Seventh Edition, the instructor guide includes
sample lecture outlines, key points, and student assignments for
every chapter in the text, along with sample laboratory exercises and
direct links to a range of detailed sources on the internet.
Test Package
The test package includes a bank of 1,609 questions created
especially for Physiology of Sport and Exercise, Seventh Edition.
Various types of questions are included: true or false, fill in the blank,
essay, and multiple choice. The test package is available for use
through multiple formats, including a learning management system,
Respondus, and rich text.
Chapter Quizzes
Updated for the seventh edition, these ready-to-use quizzes test
students’ understanding of the most important concepts in each
chapter. Chapter quizzes can be imported into learning management
systems or printed for use as written quizzes.
Presentation Package
The presentation package includes a comprehensive series of
PowerPoint slides for each chapter. Slides of learning objectives
present the major topics covered in each chapter, text slides list key
28
points, and illustration and photo slides contain graphics found in the
text. The presentation package has more than 1,000 slides that can
be used directly with PowerPoint and for printing transparencies or
slides or making copies for distribution to students. Instructors can
easily add to, modify, or rearrange the order of the slides as well as
search for slides based on key words. You may access the
presentation
package
by
visiting
www.HumanKinetics.com/PhysiologyOfSportAndExercise.
Image Bank
The image bank includes most of the illustrations, artwork, and
tables from the text, sorted by chapter. These are provided as
separate files for easy insertion into tests, quizzes, handouts, and
other course materials, which provides instructors with greater
flexibility when creating customized resources.
Instructor Video, Animations, and Audio
Within the instructor resources, the multimedia content in the web
study guide is compiled for convenient access and inclusion in
lectures and classroom presentations.
The instructor guide, test package, chapter quizzes, presentation
package, image bank, video clips, animations, and audio clips are
free to course adopters.
29
Acknowledgments
We would like to thank the staff at Human Kinetics for their continued
support of the seventh edition of Physiology of Sport and Exercise
and their dedication to publishing a high-quality product that meets
the needs of instructors and students alike. Recognition goes to Amy
Tocco (acquisitions editor) as well as our capable developmental
editors: Lori Garrett (first edition), Julie Rhoda (second and third
editions), Maggie Schwarzentraub (fourth edition), and Kate Maurer
(fifth and sixth editions); Judy Park took over the reins as
developmental editor for this seventh edition and has worked
tirelessly and expertly to keep all phases of the project on schedule
while continuing to demand the high quality for which our book is
known. They have all been a true pleasure to work with, and their
competence and skill are evident throughout the book. Special
thanks go to Joanne Brummett for her artistic expertise and
contributions to continuously improving the artwork.
For the seventh edition, special thanks also go to a handful of
colleagues who provided their valued expertise and time. In
particular, direct feedback and input from Drs. Gustavo Nader, Jinger
Gottschall, Lacy Alexander, and Jim Pawelczyk at Penn State were
invaluable in making substantive changes that not only updated and
enhance the content but also provided high quality feedback from an
instructor’s viewpoint. Special recognition goes to the “postdoc
dream team” of Drs. Jody Greaney and Anna Stanhewicz for all of
their hard work in helping update all of the Research Perspective
elements. In addition to Larry Kenney’s Penn State colleagues,
thanks also go to Dr. Bob Murray, who once again contributed his
vast knowledge about ergogenic aids to chapter 16.
Finally, we thank our families for their constant love, support, and
patience while we were writing, rewriting, editing, and proofing this
book across all seven editions.
30
W. Larry Kenney
David L. Costill
Jack H. Wilmore (posthumously)
31
Photo Credits
Chapter and part opener photos
Introduction: Echo/Juice Images/Getty Images; Part I: David
Davies/Press Association Images; Chapter 1: BSIP/Medical Images;
Chapter 2: Hero Images/DigitalVision/Getty Images; Chapter 3:
Carolina Biological/Medical Images; Chapter 4: Hank Grebe/Getty
Images; Chapter 5: Buda Mendes/Getty Images; Part II: Press
Association Images; Chapter 6: Biophoto Associates/Science
Source; Chapter 7: 3D4Medical /Medical Images; Chapter 8: Sam
Edwards/Caiaimage/Getty Images; Part III: © Human Kinetics;
Chapter 9: Alexander Hassenstein/Getty Images; Chapter 10:
Grady Reese/E+/Getty Images; Chapter 11: Alex Goodlett International Skating Union (ISU)/ISU via Getty Images; Part IV: © E
Simanor/Robert Harding Picture Library/age fotostock; Chapter 12:
Technotr/E+/Getty Images; Chapter 13: FRANCK FIFE/AFP/Getty
Images; Part V: Joshua Sarner/Icon Sportswire; Chapter 14: Hero
Images/Getty Images; Chapter 15: Sanjeri/E+/Getty Images;
Chapter 16: Simon Hausberger/Getty Images; Part VI: © Human
Kinetics; Chapter 17: Hero Images/Getty Images; Chapter 18:
Westend61/Getty Images; Chapter 19: AMR Image/E+/Getty
Images; Part VII:
©
Human
Kinetics;
Chapter
20:
FatCamera/E+/Getty
Images;
Chapter
21:
ISM
/
SOVEREIGN/Medical Images; Chapter 22: Science Photo
Library/Getty Images
Photos courtesy of the authors
Figures 0.2, 0.3, 0.4, 0.6b, 0.6c, 0.7, 0.9, 1.1, 1.11, 1.12, 1.13a,
1.13b, 5.9, 18.6, 22.7a; photos on pp. 2 (a and b)
Additional photos
32
Photo c on p. 2: Photo courtesy of Dr. Larry Golding, University of
Nevada, Las Vegas. Photographer Dr. Moh Youself; figures 0.1,
0.5a, 0.5b, and 0.6a: Photos courtesy of American College of Sports
Medicine Archives. All rights reserved; figure 0.5c: Courtesy of Noll
Laboratory, The Pennsylvania State University; figure 0.12: Andy
Cross/The Denver Post via Getty Images; figure 0.13: © Human
Kinetics; photo on p. 21: © Human Kinetics; photo in figure 1.2:
ISM/Medical Images; figure 1.4: BSIP/Medical Images; photo on p.
35: © Human Kinetics; figure 1.17b: Reprinted from J.C.
Bruusgaard et al., “Myonuclei Acquired by Overload Exercise
Precede Hypertrophy and are Not Lost on Detraining,” Proceedings
of the National Academy of Sciences 107 (2010): 15111-15116. By
permission of J.C. Bruusgaard; photo on p. 71: © Human Kinetics;
photo in figure 3.2: Carolina Biological/Medical Images; photos on
pp. 93 and 110: © Human Kinetics; photo on p. 112: Photo
courtesy of Larry Kenney; figure 5.2: © Human Kinetics; photo on
p. 142: © Human Kinetics; figure 6.16b: Westend61/Getty Images;
photo in figure 7.3: © Human Kinetics; photos on pp. 190, 194,
212, 217, and 222: © Human Kinetics; figures 9.1, 9.3, and 9.5: ©
Human Kinetics; photos on pp. 240, 242, 244, and 252: © Human
Kinetics; figure 10.2: Photos courtesy of Dr. Michael Deschene’s
laboratory; photos on pp. 259 and 262: © Human Kinetics; photo
on p. 292: Dylan Buell/Getty Images; photo in figure 12.2: Carolina
Biological/Medical Images; figure 12.3: From Department of Health
and Human Performance, Auburn University, Alabama. Courtesy of
John Eric Smith, Joe Molloy, and David D. Pascoe. By permission of
David Pascoe; photos on pp. 307 and 325: © Human Kinetics;
photo on p. 326: ©Wojciech Gajda/fotolia.com; photo on p. 369:
Photo courtesy of Larry Kenney; figure 15.2: © Human Kinetics;
figure 15.3: Photos courtesy of Hologic, Inc.; figure 15.4: David
Cooper/Toronto Star via Getty Images; figure 15.5: © Human
Kinetics; figure 15.6: Courtesy of Rice Lake Weighing Systems;
photos on pp. 454, 488, and 493: © Human Kinetics; figure 19.9:
Dee Breger/Science Source; photo on p. 505: © Human Kinetics;
figure 20.1: © Human Kinetics; figure 22.7b: ISM/ Pr Jean-Denis
LAREDO/Medical Images; photo on p. 571: © Human Kinetics
33
34
INTRODUCTION
An Introduction to Exercise and Sport
Physiology
In this chapter and in the web study guide
Focus of Exercise and Sport Physiology
Acute and Chronic Responses to Exercise
The Evolution of Exercise Physiology
Beginnings of Anatomy and Physiology
Early History of Exercise Physiology
Era of Scientific Exchange and Interaction
Development of Contemporary Approaches
Integrative Physiology
Translational Physiology
Pioneering Women in Exercise Physiology
ACTIVITY 0.1 Timeline presents a historical perspective of the history of exercise physiology.
VIDEO 0.1 presents Jim Pawelczyk discussing the integration of cellular-level processes with a view
of the entire organism.
Exercise Physiology in the 21st Century
Exercise in Personalized Medicine
The “-Omics” Revolution
Epigenetics
Bioinformatics
Exercise Physiology Beyond Earth’s Boundaries
VIDEO 0.2 presents Jim Pawelczyk discussing the four P’s of medicine and the important role of
exercise in individualized health strategies.
Research: The Foundation for Understanding
The Research Process
35
Research Settings
Research Tools: Ergometers
Research Designs
Research Controls
Confounding Factors in Exercise Research
Units and Scientific Notation
Reading and Interpreting Tables and Graphs
ANIMATION FOR FIGURE 0.11 details the process of scientific research.
AUDIO FOR FIGURE 0.14 describes a cross-sectional study design.
AUDIO FOR FIGURE 0.15 describes a longitudinal study design.
ACTIVITY 0.2 Interpreting Figures and Tables explains the components of charts, figures, and
tables and how to interpret their data.
AUDIO FOR FIGURE 0.16 describes how to interpret a line graph.
AUDIO FOR FIGURE 0.17 describes the nonlinear response pattern shown in the graph.
In Closing
36
M
uch of the history of exercise physiology in the United States can be
traced to the effort of a Kansas farm boy, David Bruce (D.B.) Dill, whose interest in
physiology first led him to study the composition of crocodile blood. Fortunately for
what would eventually grow into the discipline of exercise physiology, this young
scientist redirected his research to humans when he became the first research
director of the Harvard Fatigue Laboratory in 1927. Throughout his life he was
intrigued by the physiology and adaptability of many animals that survive extreme
exercise and environmental conditions, but he is best remembered for his research
on human responses to exercise, heat, high altitude, and other environmental
factors. Dr. Dill always served as one of the human guinea pigs in his own studies.
During the Harvard Fatigue Laboratory’s 20-year existence, he and his coworkers
produced approximately 350 scientific papers along with a classic book titled Life,
Heat, and Altitude.10
After the Harvard Fatigue Laboratory closed its doors in 1947, Dr. Dill began a
second career as deputy director of medical research for the Army Chemical
Corps, a position he held until his retirement from that post in 1961. Dr. Dill was
then 70 years old—an age he considered too young for retirement—so he moved
his research to Indiana University, where he served as a senior physiologist until
1966. In 1967 he obtained funding to establish the Desert Research Laboratory at
the University of Nevada at Las Vegas. Dr. Dill used this laboratory as a base for
his studies on human tolerance to exercise in the desert and at high altitude. He
continued his research and writing until his final retirement at age 93, the same
year he produced his last publication, titled The Hot Life of Man and Beast.11
Dr. David Bruce (D.B.) Dill (a) at the beginning of his career, (b) as director of the Harvard
Fatigue Laboratory at age 42, and (c) at age 92 just before his fourth retirement.
37
The human body is an amazing machine. As you sit reading this
introduction, countless perfectly coordinated and integrated events
are occurring simultaneously in your body. These events allow
complex functions, such as hearing, seeing, breathing, and
information processing, to continue without any conscious effort. If
you stand up, walk out the door, and jog around the block, almost all
of your body’s systems will be activated, enabling you to successfully
shift from rest to exercise. If you continue this routine regularly for
weeks or months and gradually increase the duration and intensity of
your jogging, your body will adapt so that you can perform better.
Therein lie the two basic components of the study of exercise
physiology: the acute responses of the body to exercise in all its
forms and the adaptation of the body’s systems to repeated or
chronic exercise, often called exercise training.
For example, as a point guard directs her team down the
basketball court on a fast break, her body makes many adjustments
that require a series of complex interactions involving many body
systems. Adjustments occur even at the cellular and molecular
levels. To enable the coordinated leg muscle actions as she moves
rapidly down court, nerve cells from the brain, referred to as motor
neurons, conduct electrical impulses down the spinal cord to the
legs. On reaching the muscles, these neurons release chemical
messengers that cross the gap between the nerve and muscle, each
neuron exciting a number of individual muscle cells or fibers. Once
the nerve impulses cross this gap, they spread along the length of
each muscle fiber and attach to specialized receptors. Binding of the
messenger to its receptor sets into motion a series of steps that
activate the muscle fiber’s contraction processes, which involve
specific protein molecules—actin and myosin—and an elaborate
energy system to provide the fuel necessary to sustain a single
contraction and subsequent contractions. It is at this level that other
molecules, such as adenosine triphosphate (ATP) and
phosphocreatine (PCr), become critical for providing the energy
necessary to fuel contraction.
In support of this sustained and rhythmic muscular contraction
and relaxation, multiple additional systems are called into action,
including the following:
38
The skeletal system provides the basic framework around
which muscles act.
The cardiovascular system delivers fuel to working muscle
and to all of the cells of the body and removes waste
products.
The cardiovascular and respiratory systems work together to
provide oxygen to the cells and remove carbon dioxide.
The integumentary system (skin) helps maintain body
temperature by allowing the exchange of heat between the
body and its surroundings.
The nervous and endocrine systems coordinate this activity,
while helping to maintain fluid and electrolyte balance and
assisting in the regulation of blood pressure.
For centuries, scientists have studied how the human body
functions at rest in health and disease. During the past 100 years or
so, a specialized group of physiologists have focused their studies
on how the body functions during physical activity and sport. This
introduction presents a historical overview of exercise and sport
physiology and then explains some basic concepts that form the
foundation for the chapters that follow.
Focus of Exercise and Sport Physiology
Exercise and sport physiology have evolved from the fundamental
disciplines of anatomy and physiology. Anatomy is the study of an
organism’s structure, or morphology. While anatomy focuses on the
basic structure of various body parts and their interrelationships,
physiology is the study of body function. Physiologists study how
the body’s organ systems, tissues, cells, and the molecules within
cells work and how their functions are integrated to regulate the
body’s internal environment, a process called homeostasis.
Because physiology focuses on the functions of body structures,
understanding anatomy is essential to learning physiology.
Furthermore, both anatomy and physiology rely on a working
knowledge of biology, chemistry, physics, and other basic sciences.
Exercise physiology is the study of how the body’s functions are
altered when we are physically active, since exercise presents a
39
challenge to homeostasis. Because the environment in which one
performs exercise has a large impact, environmental physiology
has emerged as a subdiscipline of exercise physiology. Sport
physiology further applies the concepts of exercise physiology to
enhancing sport performance and optimally training athletes. Thus,
sport physiology derives its principles from exercise physiology.
Because exercise physiology and sport physiology are so closely
related and integrated, it is often hard to clearly distinguish between
them. Because the same underlying scientific principles apply,
exercise and sport physiology are often considered together, as they
are in this text.
Acute and Chronic Responses to Exercise
The study of exercise and sport physiology involves learning the
concepts associated with two distinct exercise patterns. First,
exercise physiologists are concerned with how the body responds to
an individual bout of exercise, such as running on a treadmill for an
hour or lifting weights. An individual bout of exercise is called acute
exercise, and the responses to that exercise bout are referred to as
acute responses. When examining the acute response to exercise,
we are concerned with the body’s immediate response to, and
sometimes its recovery from, a single exercise bout.
The other major area of interest in exercise and sport physiology
is how the body responds over time to the stress of repeated bouts
of exercise, sometimes referred to as chronic adaptation or
training effects. When one performs regular exercise over a period
of days and weeks, the body adapts. The physiological adaptations
that occur with chronic exposure to exercise or training improve both
exercise capacity and efficiency. With resistance training, the
muscles become stronger. With aerobic training, the heart and lungs
become more efficient and endurance capacity of the muscles
increases. As discussed later in this introductory chapter and in more
detail in chapters 10 and 11, these adaptations are highly specific to
the type of training the person does.
In Review
40
Exercise physiology evolved from its parent discipline, physiology. The two
primary concerns of exercise physiology are
how the body responds to the acute stress of a single bout of exercise or
physical activity; and
how the body adapts to the chronic stress of repeated bouts of exercise—that
is, exercise training.
Some exercise physiologists use exercise or environmental conditions (heat,
cold, altitude, and so on) to stress the body in ways that uncover basic
physiological mechanisms. Others examine exercise training’s effects on health,
disease, and well-being. Sport physiologists apply these concepts to athletes and
sport performance.
The Evolution of Exercise Physiology
To students, contemporary exercise physiology may seem like a vast
collection of new ideas never before subjected to rigorous scientific
scrutiny. On the contrary, our current understanding of exercise
physiology is based on the lifelong efforts of hundreds of outstanding
scientists. The theories and hypotheses of modern physiologists
have been shaped by the efforts of scientists who may be long
forgotten. What we consider original or new is most often an
assimilation of previous findings or the application of basic science to
problems in exercise physiology. As with every discipline, there are,
of course, a number of key scientists and pivotal scientific
contributions that brought about significant advances in our
knowledge of the physiological responses to exercise. The following
section reflects on the history of the field of exercise physiology and
on a few of the people who shaped it. It is impossible in this short
section to do justice to the hundreds of pioneering scientists who
paved the way and laid the foundation for modern exercise
physiology.
Beginnings of Anatomy and Physiology
One of the earliest descriptions of human anatomy and physiology
was Claudius Galen’s Greek text De fascius, published in the first
century. As a physician to the gladiators, Galen had ample
opportunity to study and experiment on human anatomy and was a
great proponent of science based on observation and
41
experimentation. He was aware of the dire consequences of
sedentary living and linked regular exercise to overall health and
well-being by including regular exercise as one of his laws of health:
Breathe fresh air.
Eat the proper foods.
Drink the right drinks.
Exercise.
Get adequate sleep.
Have a daily bowel movement.
Control your emotions.
Galen’s theories of anatomy and physiology were so widely
accepted that they remained unchallenged for nearly 1,400 years.
Not until the 1500s were any truly significant contributions made to
the understanding of both the structure and function of the human
body. A landmark text by Andreas Vesalius, titled Fabrica Humani
Corporis [Structure of the Human Body], presented his findings on
human anatomy in 1543. Although Vesalius’ book focused primarily
on anatomical descriptions of various organs, he occasionally
attempted to explain their functions as well. British historian Sir
Michael Foster said, “This book is the beginning, not only of modern
anatomy, but of modern physiology. It ended, for all time, the long
reign of fourteen centuries of precedent and began in a true sense
the renaissance of medicine” (p. 354).14
Most early attempts at explaining physiology were either incorrect
or so vague that they could be considered no more than speculation.
Attempts to explain how a muscle generates force, for example,
were usually limited to a description of its change in size and shape
during action because observations were limited to what could be
seen with the naked eye. From such observations, Hieronymus
Fabricius (ca. 1574) suggested that a muscle’s contractile power
resided in its fibrous tendons, not in its “flesh.” Anatomists did not
discover the existence of individual muscle fibers until Dutch scientist
Antonie van Leeuwenhoek introduced the microscope (ca. 1660).
How these fibers shorten and create force would remain a mystery
42
until the middle of the 20th century, when the intricate workings of
muscle proteins could be studied by electron microscopy.
Early History of Exercise Physiology
Although exercise physiology is a relative newcomer to the world of
science, one of its first publications appeared in 1793, when a paper
by Séguin and Lavoisier described the oxygen consumption of a
young man measured both in the resting state and while he
repeatedly lifted a 7.3 kg (16 lb) weight for 15 min.26 At rest the man
used 24 L of oxygen per hour (L/h), which increased to 63 L/h during
exercise. Lavoisier believed that the site of oxygen utilization and
carbon dioxide production was in the lungs. Even though this
concept was doubted by other physiologists of the time, it remained
accepted doctrine until the middle of the 1800s, when several
German physiologists demonstrated that combustion of oxygen
occurred in cells throughout the entire body.
Although many advances in the understanding of circulation and
respiration occurred during the 1800s, few efforts were made to
focus on the physiology of physical activity. However, in 1888, an
apparatus was described that enabled scientists to study subjects
during mountain climbing, even though the subjects had to carry a 7
kg (15.4 lb) “gasometer” on their backs.31
Arguably the first published textbook on exercise physiology,
Physiology of Bodily Exercise, was written in French by Fernand
LaGrange in 1889.19 Considering the small amount of research on
exercise that had been conducted up to that time, it is intriguing to
read the author’s accounts of such topics as “Muscular Work,”
“Fatigue,” “Habituation to Work,” and “The Office of the Brain in
Exercise.” This early attempt to explain the response to exercise
was, in many ways, limited to speculation and theory. Although some
basic concepts of exercise biochemistry were emerging at that time,
LaGrange was quick to admit that many details were still in the
formative stages. For example, he stated that
Vital combustion [energy metabolism] has become very complicated of late;
we may say that it is somewhat perplexed, and that it is difficult to give in a
few words a clear and concise summary of it. It is a chapter of physiology
which is being rewritten, and we cannot at this moment formulate our
conclusions. (p. 395)19
43
Because the early text by LaGrange offered only limited
physiological insights regarding bodily functions during physical
activity, some argue that the third edition of a text by F.A. Bainbridge
titled The Physiology of Muscular Exercise, published in 1931,
should be considered the earliest scientific text on this subject.2
Interestingly, that third edition was written by A.V. Bock and D.B. Dill,
at the request of A.V. Hill, three key pioneers of exercise physiology
discussed in this introductory chapter.
Archibald V. (A.V.) Hill was a significant figure in the history of
exercise physiology. In his inaugural address as Joddrell Professor
of Physiology at University College London, Hill stated the principles
that subsequently shaped the field of exercise physiology:
It is strange how often a physiological truth discovered on an animal may be
developed and amplified, and its bearings more truly found, by attempting to
work it out on man. Man has proved, for example, far the best subject for
experiments on respiration and on the carriage of gases by the blood, and
an excellent subject for the study of kidney, muscular, cardiac and metabolic
function.… Experiment on man is a special craft requiring a special
understanding and skill, and “human physiology,” as it may be called,
deserves an equal place in the list of those main roads which are leading to
the physiology of the future. The methods, of course, are those of
biochemistry, of biophysics, of experimental physiology; but there is a special
kind of art and knowledge required of those who wish to make experiments
on themselves and their friends, the kind of skill that the athlete and the
mountaineer must possess in realizing the limits to which it is wise and
expedient to go.
During the late 1800s, many theories were proposed to explain
the source of energy for muscle contraction. Muscles were known to
generate much heat during exercise, so some theories suggested
that this heat was used directly or indirectly to cause muscle fibers to
shorten. After the turn of the century, Walter Fletcher and Sir
Frederick Gowland Hopkins observed a close relation between
muscle action and lactate formation.12 This observation led to the
realization that energy for muscle action is derived from the
breakdown of muscle glycogen to lactic acid (see chapter 2),
although the details of this reaction remained obscure. Because of
the high energy demands of exercising muscle, this tissue served as
an ideal model to help unravel the mysteries of cellular metabolism.
In 1921, A.V. Hill (figure 0.1) was awarded the Nobel Prize for his
44
findings on energy metabolism. At that time, biochemistry was in its
infancy, although it was rapidly gaining recognition through the
research efforts of such other Nobel laureates as Albert SzentGyörgyi, Otto Meyerhof, August Krogh, and Hans Krebs, all of whom
were actively studying how living cells generate and use energy.
FIGURE 0.1 1921 Nobel Prize winner Archibald V. Hill (1927).
Although much of Hill’s research was conducted with isolated frog
muscle, he also conducted some of the first physiological studies of
runners. Such studies were made possible by the technical
contributions of John S. Haldane, who developed the methods and
equipment needed to measure oxygen use during exercise. These
and other investigators provided the basic framework for our
understanding of whole-body energy production, which became the
focus of considerable research during the middle of the 20th century
and is incorporated into the manual and computer-based systems
that are used to measure oxygen uptake in exercise physiology
laboratories throughout the world today. In his address, A.V. Hill went
on to acknowledge Haldane’s contributions and discuss the wide
range of applications he saw for his work in exercise physiology:
Quite apart from direct physiological research on man, the study of
instruments and methods applicable to man, their standardization, their
description, their reduction to routine, together with the setting up of
standards of normality in man are bound to prove of great advantage to
medicine; and not only to medicine but to all those activities and arts where
normal man is the object of study. Athletics, physical training, flying, working,
45
submarines, or coal mines, all require a knowledge of the physiology of man,
as does also the study of conditions in factories. The observation of sick men
in hospitals is not the best training for the study of normal man at work. It is
necessary to build up a sound body of trained scientific opinion versed in the
study of normal man, for such trained opinion is likely to prove of the
greatest service, not merely to medicine, but in our ordinary social and
industrial life. Haldane’s unsurpassed knowledge of the human physiology of
respiration has often rendered immeasurable service to the nation in such
activities as coal mining or diving; and what is true of the human physiology
of respiration is likely also to be true of many other normal human functions.
Era of Scientific Exchange and Interaction
From the early 1900s through the 1930s, the medical and scientific
environment in the United States was changing. This was an era of
revolution in the education of medical students, led by changes at
Johns Hopkins. More medical and graduate programs based their
educational endeavors on the European model of experimentation
and development of scientific insights. There were important
advances in physiology in areas such as bioenergetics, gas
exchange, and blood chemistry that served as the basis for
advances in the physiology of exercise. Building on collaborations
forged in the late 1800s, interactions of laboratories and scientists
were promoted, and international meetings of organizations such as
the International Union of Physiological Sciences created an
atmosphere for free scientific exchange, discussion, and debate.
Research laboratories and collaborations created during this period
would go on to do some of the most important exercise physiology
research of the 20th century.
Research on Athletes
For more than 100 years, athletes have served as subjects for study
of the upper limits of human endurance. Perhaps the first
physiological studies on athletes occurred in 1871. Austin Flint
studied one of the most celebrated athletes of that era, Edward
Payson Weston, an endurance runner-walker. Flint’s investigation
involved measuring Weston’s energy balance (i.e., food intake
versus energy expenditure) during Weston’s attempt to walk 400 mi
(644 km) in 5 days. Although the study resolved few questions about
46
muscle metabolism during exercise, it did demonstrate that some
protein is lost from the body during prolonged heavy exercise.13
Throughout the 20th century, athletes were used repeatedly to
assess the physiological capabilities of human strength and
endurance and ascertain characteristics needed for record-setting
performances. Some attempts have been made to use the
technology and knowledge derived from exercise physiology to
predict performance, prescribe training, or identify athletes with
exceptional potential. In most cases, however, these applications of
physiological testing are of little more than academic interest
because few laboratory or field tests can accurately assess all the
qualities required for someone to become a champion.
The Harvard Fatigue Laboratory
Perhaps no university has had more influence on the field of
exercise physiology than Harvard. From 1891 to 1898, Harvard
offered a degree in anatomy, physiology, and physical training under
the direction of Dr. George Wells Fitz to “provide necessary
knowledge about the science of exercise.” While that department
changed its focus with Fitz’s departure in 1899, many other U.S.
universities developed programs over the next 25 years that coupled
basic science coursework with physical education.
A visit by A.V. Hill to Harvard University in 1926 had a significant
impact on the founding and early activities of the Harvard Fatigue
Laboratory (HFL), which was established a year later in 1927.
Interestingly, the early home of the HFL was the basement of
Harvard’s Business School, and its stated early mission was to
conduct research on fatigue and other hazards in industry. Creation
of this laboratory was due to the insightful planning of world-famous
biochemist Lawrence J. (L.J.) Henderson. A young biochemist from
Stanford University, David Bruce (D.B.) Dill, was appointed as the
first director of research, a title Dill held until the HFL closed in 1947.
As noted earlier, Dill had aided Arlen “Arlie” Bock in writing the
third edition of Bainbridge’s text on exercise physiology. Later in his
career Dill credited the writing of that textbook with shaping the
program of the HFL. Although he had little experience in applied
human physiology, Dill’s creative thinking and ability to surround
47
himself with young, talented scientists created an environment that
would lay the foundation for modern exercise and environmental
physiology. For example, HFL personnel examined the physiology of
endurance exercise and described the physical requirements for
success in events such as distance running. Some of the most
outstanding HFL investigations were conducted not in the laboratory
but in the Nevada desert, on the Mississippi Delta, and in the White
Mountains in California (with an altitude of 3,962 m, or 13,000 ft).
These and other studies provided the foundation for future
investigations on the effects of the environment on physical
performance and in exercise and sport physiology.
In its early years, the HFL focused primarily on general problems
of exercise, nutrition, and health. For example, the first studies on
exercise and aging were conducted in 1939 by Sid Robinson (see
figure 0.2), a student at the HFL. On the basis of his studies of
subjects ranging in age from 6 to 91 years, Robinson described the
effect of aging on maximal heart rate and oxygen uptake.24 But with
the onset of World War II, Henderson and Dill realized the HFL’s
potential contribution to the war effort, and research at the HFL took
a different direction. Harvard Fatigue Lab scientists and support
personnel were instrumental in forming new laboratories for the
Army, Navy, and Army Air Corps (now the Air Force). They also
published the methodologies necessary for relevant military
research, methods that are still in use throughout the world.
FIGURE 0.2 Sid Robinson (a) being tested by R.E. Johnson on the treadmill in the Harvard Fatigue
Laboratory and (b) as a Harvard student and athlete in 1938.
48
Today’s exercise physiology students would be amazed at the
methods and devices used in the early days of the HFL and at the
time it took to conduct research projects in those days. What is now
accomplished in milliseconds with the aid of computers and
automatic analyzers literally demanded days of effort by HFL
scientists. Measurements of oxygen uptake during exercise, for
example, required collecting expired air in Douglas bags and
analyzing it for oxygen and carbon dioxide by using a manually
operated chemical analyzer, without the help of a computer, of
course (see figure 0.3). The analysis of a single 1 min sample of
expired air required 20 to 30 min of effort by one or more laboratory
workers. Today, scientists make such measurements almost
instantaneously and with little physical effort. One must marvel at the
dedication, diligence, and hard work of the HFL’s exercise
physiology pioneers. Using the equipment and methods available at
the time, HFL scientists published approximately 350 research
papers over a 20-year period.
FIGURE 0.3 (a) Early measurements of metabolic responses to exercise required the collection of
expired air in a sealed bag known as a Douglas bag. (b) A sample of that gas then was measured for
oxygen and carbon dioxide using a chemical gas analyzer, as illustrated by this photo of Nobel laureate
August Krogh.
The HFL was an intellectual environment that attracted young
physiologists and physiology doctoral students from all over the
globe. Scholars from 15 countries worked in the HFL between 1927
and its closure in 1947. Most went on to develop their own
laboratories and become noteworthy figures in exercise physiology
in the United States, including Sid Robinson, Henry Longstreet
Taylor, Lawrence Morehouse, Robert E. Johnson, Ancel Keys,
Steven Horvath, C. Frank Consolazio, and William H. Forbes.
49
Notable international scientists who spent time at the HFL included
August Krogh, Lucien Brouha, Edward Adolph, Walter B. Cannon,
Peter Scholander, and Rodolfo Margaria, along with several other
notable Scandinavian scientists discussed later. Thus, the HFL
planted seeds of intellect at home and around the world that resulted
in an explosion of knowledge and interest in this new field. Most
contemporary exercise physiologists can trace the roots of their
research training back to the HFL.
Scandinavian Influence
In 1909, Johannes Lindberg established a laboratory that became a
fertile breeding ground for scientific contributions at the University of
Copenhagen in Denmark. Lindberg and 1920 Nobel Prize winner
August Krogh teamed up to conduct many classic experiments and
published seminal papers on topics ranging from the metabolic fuels
for muscle to gas exchange in the lungs. This work was continued
from the 1930s into the 1970s by Erik Hohwü-Christensen, Erling
Asmussen, and Marius Nielsen.
As a result of contacts between D.B. Dill and August Krogh, these
three Danish physiologists came to the HFL in the 1930s, where they
studied exercise in hot environments and at high altitude. After
returning to Europe, each man established a separate line of
research. Asmussen and Nielsen became professors at the
University of Copenhagen, where Asmussen studied the mechanical
properties of muscle and Nielsen conducted studies on control of
body temperature. Both remained active at the University of
Copenhagen’s August Krogh Institute until their retirements.
50
FIGURE 0.4 (a) Erik Hohwü-Christensen was the first physiology professor at the College of Physical
Education at Gymnastik-och Idrottshögskolan in Stockholm, Sweden. (b) Bengt Saltin, winner of the
2002 Olympic Prize. (c) Jonas Bergstrom (left) and Eric Hultman (right) were the first to use muscle
biopsy to study muscle glycogen use and restoration before, during, and after exercise.
In 1941, Hohwü-Christensen (see figure 0.4a) moved to
Stockholm, Sweden, to become the first physiology professor at the
College of Physical Education at Gymnastik-och Idrottshögskolan
(GIH). In the late 1930s, he teamed with Ole Hansen to conduct and
publish a series of five studies of carbohydrate and fat metabolism
during exercise. These studies are still cited frequently and are
considered to be among the first and most important sport nutrition
studies. Hohwü-Christensen introduced Per-Olof Åstrand to the field
of exercise physiology. Åstrand, who conducted numerous studies
related to physical fitness and endurance capacity during the 1950s
and 1960s, became the director of GIH after Hohwü-Christensen
retired in 1960. During his tenure at GIH, Hohwü-Christensen
mentored a number of outstanding scientists, including Bengt Saltin,
who was the 2002 Olympic Prize winner for his many contributions to
the field of exercise and clinical physiology (see figure 0.4b).
In addition to their work at GIH, both Hohwü-Christensen and
Åstrand interacted with physiologists at the Karolinska Institute in
Stockholm, Sweden, who studied clinical applications of exercise. It
is hard to single out the most exceptional contributions from this
institute, but Jonas Bergstrom’s (figure 0.4c) reintroduction of the
biopsy needle (ca. 1966) to sample muscle tissue was a pivotal point
51
in the study of human muscle biochemistry and muscle nutrition.
This technique, which involves withdrawing a tiny sample of muscle
tissue with a needle inserted into the muscle through a small
incision, was originally introduced in the early 1900s to study
muscular dystrophy. The needle biopsy enabled physiologists to
conduct histological and biochemical studies of human muscle
before, during, and after exercise.
Other invasive studies of blood circulation were subsequently
conducted by physiologists at GIH and at the Karolinska Institute.
Just as the HFL had been the mecca of exercise physiology
research between 1927 and 1947, the Scandinavian laboratories
were equally noteworthy beginning in the late 1940s. Many leading
investigations over the following 35 years were collaborations
between American and Scandinavian exercise physiologists.
Norwegian Per Scholander introduced a gas analyzer in 1947. Finn
Martti Karvonen published a formula for calculating exercise heart
rate that is still widely used today.
Other Research Milestones
Physiology has always been the basis for clinical medicine. In the
same way, exercise physiology has provided essential knowledge for
many other areas, such as physical education, physical fitness,
physical therapy, and health promotion. In the late 1800s and early
1900s, physicians such as Amherst College’s Edward Hitchcock, Jr.
and Harvard’s Dudley Sargent studied body proportions
(anthropometry) and the effects of physical training on strength and
endurance. Although a number of physical educators introduced
biological science to the undergraduate physical education
curriculum, Peter Karpovich, a Russian immigrant who had been
briefly associated with the HFL (figure 0.5a), played a major role in
introducing physiology to physical education. Karpovich established
his own research facility and taught physiology at Springfield College
(Massachusetts) from 1927 until his death in 1968.
Although he made numerous contributions to physical education
and exercise physiology research, he is best remembered for the
outstanding students he advised, including Charles Tipton and
52
Loring Rowell, both recipients of the American College of Sports
Medicine Honor and Citation Awards.
Another Springfield faculty member, swim coach Thomas K. (T.K.)
Cureton (figure 0.5b), created an exercise physiology laboratory at
the University of Illinois at Urbana-Champaign in 1941. He continued
his research and taught many of today’s leaders in physical fitness
and exercise physiology until his retirement in 1971. Physical fitness
programs developed by Cureton and his students, as well as
Kenneth Cooper’s 1968 book, Aerobics, established a physiological
rationale for using exercise to promote a healthy lifestyle.9
FIGURE 0.5 (a) Peter Karpovich introduced the field of exercise physiology during his tenure at
Springfield College. (b) Thomas K. Cureton directed the exercise physiology laboratory at the
University of Illinois at Urbana-Champaign from 1941 to 1971. (c) At Penn State, Elsworth Buskirk
founded an intercollege graduate program focusing on applied physiology (1966) and constructed The
Laboratory for Human Performance Research (1974).
Another contributor to the establishment of exercise physiology as
an academic endeavor was Elsworth R. “Buz” Buskirk (figure 0.5c).
After holding positions as chief of the environmental physiology
section at the Quartermaster Research and Development Center in
Natick, Massachusetts (1954-1957), and research physiologist at the
National Institutes of Health (1957-1963), Buskirk moved to
Pennsylvania State University, where he stayed for the remainder of
his career. At Penn State, Buz founded the Intercollege Graduate
Program in Physiology (1966) and constructed The Laboratory for
Human Performance Research (1974), the nation’s first freestanding
research institute devoted to the study of human adaptation to
53
exercise and environmental stress. He remained an active scholar
until his death in April of 2010.
Although there was some awareness as early as the mid-1800s of
a need for regular physical activity to maintain optimal health, this
idea did not gain popular acceptance until the late 1960s.
Subsequent research has continued to support the importance of
exercise in slowing the physical decline associated with aging,
preventing or mitigating the problems associated with chronic
diseases, and rehabilitating injuries.
Development of Contemporary Approaches
Much advancement in exercise physiology must be credited to
improvements in technology. In the late 1950s, Henry L. Taylor and
Elsworth R. Buskirk published two seminal papers6,28 describing the
criteria for measuring maximal oxygen uptake and establishing that
measure as the gold standard for cardiorespiratory fitness. In the
1960s, development of electronic analyzers to measure respiratory
gases made studying energy metabolism much easier and more
productive than before. This technology and radio telemetry (which
uses radio-transmitted signals), used to monitor heart rate and body
temperature during exercise, were developed as a result of the U.S.
space program. Although such instruments took much of the labor
out of research, they did not alter the direction of scientific inquiry.
Until the late 1960s, most exercise physiology studies focused on
the whole body’s response to exercise. The majority of investigations
involved measurements of such variables as oxygen uptake, heart
rate, body temperature, and sweat rate. Cellular responses to
exercise received little attention.
Biochemical Approaches
In the mid-1960s, three biochemists emerged who were to have a
major impact on the field of exercise physiology. John Holloszy
(figure 0.6a) at Washington University in St. Louis, Missouri, Charles
“Tip” Tipton (figure 0.6b) at the University of Iowa, and Phil Gollnick
(figure 0.6c) at Washington State University first used rats and mice
to study muscle metabolism and examine factors related to fatigue.
Their publications and their training of graduate and postdoctoral
students resulted in a more biochemical approach to exercise
54
physiology research. Holloszy was ultimately awarded the 2000
Olympic Prize for his contributions to exercise physiology and health.
Before the 1960s, there were few biochemical studies on the
adaptations of muscle to training. Although the field of biochemistry
can be traced to the early part of the 20th century, this special area
of chemistry was not applied to human muscle until Bergstrom and
Hultman reintroduced and popularized the needle biopsy procedure
in 1966. Initially, this procedure was used to examine glycogen
depletion during exhaustive exercise and its resynthesis during
recovery. In the early 1970s, as noted earlier, a number of exercise
physiologists used the muscle biopsy method, histological staining,
and the light microscope to determine human muscle fiber types.
FIGURE 0.6 (a) John Holloszy was the winner of the 2000 Olympic Prize for scientific contributions in
the field of exercise science. (b) Charles Tipton was a professor at the University of Iowa and the
University of Arizona and a mentor to many students who have become the leaders in molecular
biology and genomics. (c) Phil Gollnick conducted muscle and biochemical research at Washington
State University.
Around the time Bergstrom reintroduced the needle biopsy
procedure, exercise physiologists who were well trained as
biochemists emerged. In Stockholm, Bengt Saltin realized the value
of this procedure for studying human muscle structure and
biochemistry. He first collaborated with Bergstrom in the late 1960s
to study the effects of diet on muscle endurance and muscle
nutrition. About the same time, Reggie Edgerton (University of
California at Los Angeles) and Phil Gollnick were using rats to study
the characteristics of individual muscle fibers and their responses to
training. Saltin subsequently combined his knowledge of the biopsy
55
procedure with Gollnick’s biochemical talents. These researchers
were responsible for many early studies on human muscle fiber’s
characteristics and use during exercise. Although many biochemists
have used exercise to study metabolism, few have had more impact
on the current direction of human exercise physiology than
Bergstrom, Saltin, Tipton, Holloszy, and Gollnick.
Other Tools and Techniques
The history of exercise physiology has, in some ways, been driven
by advancements in technologies adapted from basic sciences. The
early studies of energy metabolism during exercise were made
possible by the invention of gas-collecting equipment and chemical
analysis of oxygen and carbon dioxide. Chemical determination of
blood lactic acid seemed to provide some insights regarding the
aerobic and anaerobic aspects of muscular activity, but these data
told us little regarding the production and removal of this by-product
of exercise. Likewise, blood glucose measurements taken before,
during, and after exhaustive exercise proved to be interesting data
but were of limited value for understanding the energy exchange at
the cellular level.
Over the last 30 years, muscle physiologists have used various
chemical procedures to understand how muscles generate energy
and adapt to training. Test tube experiments (in vitro) with muscle
biopsy samples have been used to measure muscle proteins
(enzymes) and determine the muscle fiber’s capacity to use oxygen.
Although these studies provided a snapshot of the fiber’s potential to
generate energy, they often left more questions than answers. It was
natural, therefore, for the sciences of cell biology to move to an even
deeper level. It was apparent that the answers to those questions
must lie within the fiber’s molecular makeup.
Although not a new science, molecular biology has become a
useful tool for exercise physiologists who wish to delve more deeply
into the cellular regulation of metabolism and adaptations to the
stress of exercise. Physiologists like Frank Booth and Ken Baldwin
(figure 0.7) have dedicated their careers to understanding the
molecular regulation of muscle fiber characteristics and function and
have laid the groundwork for our current understanding of the
56
genetic controls of muscle growth and atrophy. The use of molecular
biological techniques to study the contractile characteristics of single
muscle fibers is discussed in chapter 1.
Well before James Watson and Francis Crick unraveled the
structure of deoxyribonucleic acid (DNA) in 1953, scientists
appreciated the importance of genetics in predetermining the
structure and function of all living organisms. The newest frontier in
exercise physiology combines the study of molecular biology and
genetics. Since the early 1990s, scientists have attempted to explain
how exercise causes signals that affect the expression of genes
within skeletal muscle.
FIGURE 0.7 (a) Frank Booth and (b) Ken Baldwin.
In retrospect, it is apparent that since the beginning of the 20th
century, the field of exercise physiology has evolved from measuring
whole-body function (i.e., oxygen consumption, respiration, and
heart rate) to molecular studies of muscle fiber genetic expression.
There is little doubt that exercise physiologists of the future will need
to be well grounded in biochemistry, molecular biology, and genetics.
Integrative Physiology
57
VIDEO 0.1 Presents Jim Pawelczyk discussing the integration of
cellular-level processes with a view of the entire organism.
With the announcement of the sequencing of the human genome in
2001, it was hoped that one day, scientists could simply analyze
cheek cells from a mouth swab and, by looking at your gene
sequence, predict whether you were at risk for developing diabetes
or cardiovascular disease.7,8 More promising was the idea that
detection of these predictive genetic variations could aid in
developing more effective treatments for these debilitating diseases.
These advances in biotechnology have produced huge volumes
of data over the past several years, but the initial optimism regarding
the prediction and treatment of human disease has not been
fulfilled.17 While there are a few specific gene mutations that have
reliable predictive power, such as the breast cancer gene BRCA1,
the translation of genetic technologies into predictive diagnostics or
therapies has largely not occurred. In fact, analysis of traditional risk
factors still has much more predictive power for evaluating risk for
type 2 diabetes than the evaluation of genetic risk scores based on
20 different gene variants associated with this disease.27
In the era of mega-genomic data, where does the study of
physiology fit in? And is it still relevant to human health and disease?
One outspoken advocate for the field of integrative physiology is
Dr. Michael J. Joyner. Dr. Joyner is an award-winning, distinguished
investigator at the Mayo Clinic who has critically questioned the
functional value of so-called reductionist thinking in molecular
biology. In contrast to examining biological processes at the lowest
58
common level (for example, how genes code for proteins in cells),
integrative physiology examines how whole organisms function and
adapt to internal and external stresses (including exercise). This
approach is informed by the concepts of homeostasis, regulated
organ systems, and redundancy in physiological systems. Moreover,
integrative physiologists strive to ask hypothesis-driven research
questions and design defensible experiments to test those
hypotheses.
The importance of seeking to study biological questions from an
integrative, regulated approach is highlighted by the influences of
culture, environment, and behavior on disease pathology. The
challenge for integrative physiologists is to incorporate key findings
from genetics and molecular biology and to examine how behavioral
patterns, including physical activity, diet, and stress, interplay with
this genetic variation to affect health and disease.
Translational Physiology
Exercise physiologists, by the nature of the topics we study and the
variety of approaches we use in those studies, make valuable
contributions to what has become known as translational
physiology. Translational physiology is a term that was originally
used in the early 1990s to refer to the research process needed to
link cancer risk with its predisposing genetic factors.25 The field of
translational physiology has broadened substantially from that time
to include the processes by which basic research findings are
extended to the clinical research setting, then to the realm of clinical
practice, and finally to health policy (figure 0.8). This translational
research continuum, however, works best in a bidirectional manner,
such that population-based problems, like obesity, also drive the
basic research questions that exercise physiologists ask. In turn,
these basic research findings eventually drive changes in clinical
practice and overall community health.
59
FIGURE 0.8 Flow chart for translational physiology.
Adapted from Seals (2013).
A good example of opportunities in translational physiology is in
the field of aging. Advancing age by itself is a risk factor for many
chronic diseases and presents a significant challenge to our health
care system and to society in general. In order to fully understand
the underlying physiology of aging and be able to engage in
appropriate interventions to keep the aging population healthy, we
must understand the aging process from the molecular level all the
way to the community and population levels. Being able to
successfully contribute to the translational physiology process
requires a broad skill set to critically examine data and approach
scientific problems with new goals in mind, from bench to bedside
and from bedside to community.
In Review
In an era that seems to stress a reductionist (genes, molecules) approach to
science, there is an acute need for exercise physiologists to continue to study
biological questions from an integrative, hypothesis-driven approach.
The field of translational physiology addresses the processes by which basic
research findings are extended to the clinical research setting, then to the realm
of clinical practice, and finally to health policy.
Pioneering Women in Exercise Physiology
60
While outstanding female exercise physiologists are now
commonplace, as in many areas of science, the contributions of
women to exercise physiology were slow to gain recognition. In
1954, Irma Rhyming collaborated with her future husband, P.-O.
Åstrand, to publish a classic study that provided a means to predict
aerobic capacity from submaximal heart rate.1 Although this indirect
method of assessing physical fitness has been challenged over the
years, its basic concept is still in use today.
In the 1970s, two Swedish women, Birgitta Essén and Karen Piehl
(figure 0.9), gained international attention for their research on
human muscle fiber composition and function. Essen, who
collaborated with Bengt Saltin, was instrumental in adapting
microbiochemical methods to study the small amounts of tissue
obtained with the needle biopsy procedure. Her efforts enabled
others to conduct studies on the muscle’s use of carbohydrates and
fats and to identify different muscle fiber types. Piehl published a
number of studies that illustrated which muscle fiber types were
activated during both aerobic and anaerobic exercise.
FIGURE 0.9 (a) Birgitta Essén collaborated with Bengt Saltin and Phil Gollnick in publishing the
earliest studies on muscle fiber types in human muscle. (b) Karen Piehl was among the first
physiologists to demonstrate that the nervous system selectively recruits type I (slow-twitch) and type II
(fast-twitch) fibers during exercise of differing intensities. (c) Barbara Drinkwater was among the first to
conduct studies on female athletes and to address issues specifically related to the female athlete.
In the 1970s and 1980s, a third Scandinavian female physiologist,
Bodil Nielsen, daughter of Marius Nielsen, actively conducted
studies on human responses to environmental heat stress and
dehydration. Her studies even encompassed measurements of body
temperature during immersion in water. At about the same time, an
61
American exercise physiologist, Barbara Drinkwater (figure 0.9c),
was doing similar work at the University of California at Santa
Barbara. Her studies were often conducted in collaboration with
Steven Horvath, D.B. Dill’s son-in-law and director of the UCSB’s
environmental physiology laboratory. Drinkwater’s contributions to
environmental physiology and study of the physiological problems
confronting the female athlete gained international recognition. In
addition to their scientific contributions, the legacy of these and other
women in physiology includes the credibility they earned and the
roles they played in attracting other young women to the fields of
exercise physiology and medicine.
The intent of this section has been to provide readers with an
overview of the personalities and technologies that have helped to
shape the field of exercise physiology. Naturally, a comprehensive
review of all the scientists and research associated with this field is
not possible in a text intended as an introduction to exercise
physiology, but for those students who wish to take an in-depth look
at the historical background in exercise physiology, there are several
good sources. Now that we understand the historical basis for the
discipline of exercise physiology, from which sport physiology
emerged, we can explore some basic principles of, and tools used
in, exercise and sport physiology.
Exercise Physiology in the 21st Century
The field of exercise physiology is rapidly evolving. Ever-expanding
technological developments and new approaches to science have
substantial implications for health, medicine, and biomedical
research. Exercise physiology and our understanding of the
physiological processes that underpin physical activity are often at
the forefront of this new age of science.
Exercise in Personalized Medicine
VIDEO 0.2 Presents Jim Pawelczyk discussing the four P’s of
medicine and the important role of exercise in individualized health
strategies.
62
In 2007, the United States Congress passed the Genomics and
Personalized Medicine Act. The intent of this legislation was to
implement and support research related to formulating a
personalized prescription to fit each patient’s unique genetic and
environmental characteristics in order to optimize health care
strategies.15,16 This personalized medicine concept first emerged in
the field known as pharmacogenomics, which provided scientific
insights into why some individuals respond favorably to certain drugs
while others do not respond (or may even respond adversely). For
example, studies have identified two different genes that influence
an individual’s ability to metabolize the blood thinner warfarin and
make it possible for a physician to prescribe an appropriate dosage
to optimize the drug’s therapeutic effectiveness for each individual
patient.29
Similarly, there has been a recent push to personalize each
individual’s exercise prescription.5 Exercise is a powerful intervention
for the treatment of many different medical conditions—
cardiovascular disease, diabetes mellitus, osteoporosis, metabolic
diseases, and many more. However, there is significant
heterogeneity or variability in people’s abilities to perform exercise
and adapt to the effects of exercise training,21 especially in
individuals with different clinical disease manifestations. Moreover,
researchers are just beginning to understand and formulate optimal
training programs or personalized dosages of exercise to produce
beneficial responses in these patients.
Researchers are designing experimental paradigms to determine
(1) the mechanisms through which exercise produces effects (either
positive or negative) on a cellular and systems level, (2) the optimal
63
dosage of exercise to produce results in different clinical populations,
(3) the best way to evaluate a person’s responses to exercise on an
individual and a group level, and (4) the benefit of adding exercise
therapy to existing disease treatment strategies. Part of the
challenge in personalizing exercise medicine is to understand, on a
genomic and systems level, the mechanisms responsible for the
huge variability in individuals’ responses to exercise training.
Eventually, the long-term outcomes from large randomized clinical
trials examining intraindividual variability in responses to exercise in
humans will make it possible to develop personalized strategies to
be implemented in preventive health care interventions,5 including
the health benefits of regular exercise.
The “-Omics” Revolution
As a part of the Human Genome Project, scientists sequenced all
3.2 billion nucleotides that compose the human genome. This was
mostly completed in 2003 (the last chromosome was sequenced in
2006) at an estimated cost of $2.7 billion. Today, the entire human
genome can be sequenced for less than $1,000. This has opened up
new fields of science, often called -omics. This new research area in
turn has fostered the development of new technologies aimed at the
universal detection of gene sequences and variants (genomics), the
expression of genes at the messenger RNA (mRNA) level
(transcriptomics), the proteins that are produced (proteomics), and
other products of metabolic reactions (i.e., metabolites, studied in
metabolomics)30 involved in all aspects of physiological function (see
figure 0.10). One purported appeal of -omics research is that a highly
complex system (e.g., the exercising human) can be more fully
understood if it is examined at each of the most basic levels of
inquiry. As it is applied to exercise physiology, the primary goal of omics research is to illuminate exercise physiology and behavior in
order to better understand the preventive and therapeutic values of
exercise.4
Exercise genomics research examines the role of individual (or
groups of) genes in modifying the impact of exercise training and
physical activity on performance and health- and fitness-related
traits. This is based on accumulating evidence that variations within
64
the DNA sequences (called single nucleotide polymorphisms, or
SNPs) of one or more genes may contribute to differences in
exercise behavior, cardiorespiratory and muscular fitness,
cardiovascular and metabolic function during acute exercise, and
adaptations to exercise training.3
FIGURE 0.10 The link between genomics, transcriptomics, proteomics, and metabolomics in the
context of exercise physiology.
Using genomics approaches, researchers are also attempting to
examine the genetic basis of these highly complex traits by
examining tissue-specific mRNA levels. The technologies used to
confirm a gene target and define its biological function are
increasingly sophisticated and now include DNA and RNA
sequencing, in vitro cell-based investigations, genetic modifications
in animal models, and selective breeding of animals for extreme
performance traits to identify target genes and their variants.
More recently, researchers have started to combine genomics and
transcriptomics. That is, by examining the RNA strands produced
during transcription (transcript abundance) in relevant tissues,
researchers can predict a certain trait and identify gene targets for
65
subsequent genomics research. These new gene targets can then
be probed for their DNA sequence variants and their relation with
other traits of interest. This integrated strategy within the -omics
world has the potential to expand our understanding of exercise
physiology at a level of detail that was not possible in the past. For
example, understanding the exercise training–induced alterations in
gene expression may provide novel candidates for genomics and
genetics research aimed at further understanding the physiology of
exercise.3
Exercise proteomics aims to study the entire protein content of a
biological tissue in a particular situation (e.g., immediately after a
resistance training session) or over a predetermined period (e.g.,
before and after months of endurance training), enabling
investigators to examine the molecular mechanisms that underlie
physiological adaptations to exercise.22 The original tool for
proteomic analysis was a procedure called two-dimensional
polyacrylamide gel electrophoresis. During the current genomic
research era, these gel-based methodologies have continued to
improve and are now being coupled with newer techniques based on
protein labeling, peptide fragmentation, and high-throughput mass
spectrometry to improve proteomic analyses. Research combining
proteomic data with the genomic approaches described previously
will continue to expand our understanding of exercise physiology by
providing a big picture of how exercise affects the various organs
and systems in the body to improve physiological function, exercise
performance, and health in general.
Epigenetics
It is now apparent that exercise alters gene expression, expression
of transcription factors, and other regulatory proteins. These
exercise-induced alterations have functional consequences at many
levels, including metabolism, cardiovascular regulation, and fitness
in general. However, more mechanisms and more tissues are likely
involved in the integrative response to habitual exercise.
Epigenetics is the study of changes in gene expression that occur
without changing the genetic code itself. For example, inherited
factors clearly influence an individual’s response to exercise.
66
However, additional environmental factors can alter those genes by
epigenetic modifications, which are changes in how genes function
that do not change the nucleotide sequence of the genes
themselves. Environmental stimuli can alter the epigenome in a
stable and inheritable fashion. Epigenetic modifications include DNA
methylation, histone modification, and noncoding RNAs.20 Although
this area of research is relatively new, recent studies have
demonstrated that epigenetic modifications contribute to altered
gene expression in response to regular exercise; these findings have
implications for improving our understanding of exercise-induced
health benefits. The field of exercise epigenetics is still in its infancy
but will increasingly provide new insights into human adaptations to
exercise.
Bioinformatics
The techniques described in the previous sections generate an
enormous amount of complex data. Sophisticated technologies,
computer software, and statistical methods are therefore critical to
analyzing the vast amount of genetic and molecular data generated
from a single study, not to mention the integration of information from
tens, hundreds, or thousands of experiments. Bioinformatics is
essentially the management information system for molecular
biology, serving as an intersection between molecular data and
advanced mathematical and statistical approaches.18
Bioinformatics techniques allow us to address physiological
questions that are otherwise unattainable using conventional
methods. Using robotics, software for data processing and control,
liquid handling devices, and sensitive detectors, high-throughput
biology allows researchers to quickly conduct millions of chemical,
genetic, or pharmacological tests by automating experiments on a
large scale. By doing this, it becomes feasible to repeat experiments
thousands of times. Using high-throughput methods, we can rapidly
identify active compounds, antibodies, or genes that control or alter a
particular physiological pathway.
Over the past decade, much has been learned from applying omics approaches to the field of exercise physiology, and as this
area of research continues to advance, bioinformatics will continue
67
to play a role. The development of software-based analyses that
would consider the genetic profile of an individual and then predict
his or her response to aerobic exercise training is one example of a
potential application of bioinformatics and functional -omics in
exercise physiology. As more and more research laboratories begin
to incorporate -omics approaches in exercise physiology, the need
for the bioinformatics tools to analyze and interpret the data will only
increase.
One of the main goals of exercise physiology in the 21st century is
to map function from genotype (the genetic makeup of an individual)
to phenotype (observable characteristics of an individual resulting
from the interaction of its genotype with the environment). In
essence, exercise is a powerful stimulus that influences gene
transcription across multiple tissues with implications for multiple
phenotypes. It is tempting to speculate that, in the future, perhaps a
person’s genotype will be fed into an algorithm that can make
predictions about exercise-related attributes, such as endurance,
speed, strength, or adaptability. From there, an individualized and
optimized training program could be developed.
However, it is important to remember that, while these reductionist
methods and -omics approaches have provided important new
information about the genes and pathways that underlie the
physiological responses to exercise, a much more comprehensive
understanding of the complex interaction among various genetic and
epigenetic factors is required to fully optimize the use of exercise for
disease prevention and treatment.
Exercise Physiology Beyond Earth’s Boundaries
An important segment of exercise physiology concerns the response
and adaptation of people to extremes of heat, cold, and altitude.
Understanding and controlling the physiological stresses and
adaptations that occur at these environmental limits have contributed
directly to notable societal achievements such as construction of the
Brooklyn Bridge, the Hoover Dam, pressurized aircraft, and
underwater habitats for the commercial diving industry.
The next generation of environmental challenges will also require
such physiological expertise. Commercial space vehicles now travel
68
routinely to low Earth orbit. NASA recently announced a set of new
initiatives that will place humans in deep orbits near the moon in the
late 2020s, followed by regular trips to Martian orbit in the 2030s.
Indeed, we are on the verge of becoming an interplanetary
civilization!
There are tremendous physiological and psychological challenges
imposed on humans living in space and on planetary bodies for
extended periods of time. The continuous pull of gravity contributes
to the growth and adaptation of postural skeletal muscles, loads
bones, which increases their size and density, and requires the
cardiovascular system to maintain blood pressure and brain blood
flow. In a microgravity environment (free fall around the Earth or
constant-velocity conditions in deep space), the reduction in loading
leads to dramatic losses in muscle mass and strength, osteoporosis,
and exercise intolerance at rates that mimic those seen in spinal
cord–injured patients.
Beginning in the 1980s, experiments done aboard a series of
dedicated space shuttle flights investigated these problems in detail.
The National Aeronautics and Space Administration (NASA) began
flying the European Space Agency–developed Spacelab module,
ushering in a new era of internationally sponsored scientific research
into low Earth orbit. The Spacelab Life Sciences (SLS-1, SLS-2)
missions (STS-40 and STS-58) emphasized the study of
cardiorespiratory, vestibular, and musculoskeletal adaptations to
microgravity, and the Life and Microgravity Sciences mission (STS78) concentrated on neuromuscular adaptation. The 1998 Neurolab
mission (STS-90), with an exclusive neuroscience theme, concluded
flights of the Spacelab module. Dr. James A. Pawelczyk, a Penn
State exercise physiologist and payload specialist on that flight,
cotaught the first exercise physiology class from space!
With the end of the space shuttle program, work continues today
aboard the International Space Station, which has provided a
continuous human presence in space for nearly 20 years. The tools
of modern molecular biology are helping to elucidate how loading,
radiation, and stress interact to affect all physiological systems.
For the exercise physiologist, the question is what combination of
resistance and aerobic exercise training can prevent or diminish the
69
changes that occur during space exploration. At this time, the
answer is not complete. Furthermore, if physical conditioning is
required before, during, and after space missions that could last up
to 30 months, how should exercise prescriptions be individualized,
evaluated, and updated? Without doubt, further research in exercise
and environmental physiology will be essential to complete what is
destined to be the largest exploration feat of the 21st century.
Research: The Foundation for Understanding
Exercise and sport scientists actively engage in research to better
understand the mechanisms that regulate the body’s physiological
responses to acute bouts of exercise, as well as its adaptations to
training and detraining. Most of this research is conducted at major
research universities, medical centers, and specialized institutes
using standardized research approaches and select tools of the
exercise physiologist.
The Research Process
Science and research (the process by which science is developed)
involve a process designed to pose and answer appropriate
questions, develop testable hypotheses, test those hypotheses
appropriately, generate usable data, interpret those data, and either
accept or refute the original hypotheses. The research process is
illustrated in figure 0.11. Scientists are constantly challenged to
make careful observations either from nature or the scientific
literature, then ask focused questions that can be examined using a
well-designed and well-controlled experimental process. The usual
result of this overall process is submitting a research manuscript to
an appropriate scientific journal, where it is peer reviewed, revised,
and (hopefully) published. As other scientists read the research
paper, they may in turn craft their own follow-up questions, and the
process continues.
70
FIGURE 0.11 A simplified diagram of the typical process involved in scientific research.
Research Settings
Research can be conducted either in the laboratory or the field.
Laboratory tests are usually more accurate because more
specialized and sophisticated equipment can be used and conditions
can be carefully controlled. As an example, the direct laboratory
measurement of maximal oxygen uptake ( O2max) is considered the
most accurate estimate of cardiorespiratory endurance capacity.
However, some field tests, such as the 1.5 mi (2.4 km) run, are also
used to estimate O2max. These field tests, which measure the time it
takes to run a set distance or the distance that can be covered in a
fixed time, are not totally accurate, but they provide a reasonable
estimate of O2max, are inexpensive to conduct, and allow many
people to be tested in a short time. Field tests can be conducted in
the workplace, on a running track or in a swimming pool, or during
athletic competitions. To measure O2max directly and accurately,
one would need to go to a university or clinical laboratory.
71
Research Tools: Ergometers
When physiological responses to exercise are assessed in a
laboratory setting, the participant’s physical effort must be controlled
to provide a measurable exercise intensity. This is generally
accomplished through use of ergometers. An ergometer (ergo =
work; meter = measure) is an exercise device that allows the
intensity of exercise to be controlled (standardized) and measured.
Treadmills
Treadmills are the ergometers of choice for most researchers and
clinicians, particularly in the United States. With these devices, a
motor drives a large belt on which a subject can either walk or run;
thus, these ergometers are often called motor-driven treadmills (see
figure 0.12). Belt length and width must accommodate the
individual’s body size and stride length. For example, it is nearly
impossible to test elite athletes on treadmills that are too short, or
obese subjects on treadmills that are too narrow or not sturdy
enough.
Treadmills offer a number of advantages. Walking is a natural
activity for almost everyone, so individuals normally adjust to the skill
required for walking on a treadmill within a few minutes. Also, most
people can achieve their peak values for most physiological
variables (heart rate, ventilation, oxygen uptake) on the treadmill,
although some athletes (e.g., competitive cyclists) achieve higher
values on ergometers that more closely match their mode of training
or competition.
72
FIGURE 0.12 A motor-driven treadmill.
Treadmills do have some disadvantages. They are generally more
expensive than simpler ergometers, like the cycle ergometers
discussed next. They are also bulky, require electrical power, and
are not very portable. Accurate measurement of blood pressure
during treadmill exercise can be difficult because both the noise
associated with normal treadmill operation and subject movement
can make hearing through a stethoscope difficult.
Cycle Ergometers
For many years, the cycle ergometer was the primary testing
device in use, and it is still used extensively in both research and
clinical settings. Cycle ergometers can be designed to allow subjects
to pedal either in the normal upright position (see figure 0.13) or in
reclining or semireclining positions.
Cycle ergometers in a research setting generally use either
mechanical friction or electrical resistance. With mechanical friction
devices, a belt encompassing a flywheel is tightened or loosened to
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adjust the resistance against which the cyclist pedals. The power
output depends on the combination of the resistance and the
pedaling rate—the faster one pedals, the greater the power output.
To maintain the same power output throughout the test, one must
maintain the same pedaling rate, so pedaling rate must be constantly
monitored.
FIGURE 0.13 A cycle ergometer.
With electrically braked cycle ergometers, the resistance to
pedaling is provided by an electrical conductor that moves through a
magnetic or electromagnetic field. The strength of the magnetic field
determines the resistance to pedaling. These ergometers can be
controlled so that the resistance increases automatically as pedal
rate decreases, and decreases as pedal rate increases, to provide a
constant power output.
Similar to treadmills, cycle ergometers offer some advantages and
disadvantages compared to other ergometers. Exercise intensity on
a cycle ergometer does not depend on the subject’s body weight.
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This is important when one is investigating physiological responses
to a standard rate of work (power output). As an example, if
someone lost 5 kg (11 lb), data derived from treadmill testing could
not be compared with data obtained before the weight loss because
physiological responses to a set speed and grade on the treadmill
vary with body weight. After the weight loss, the rate of work at the
same speed and grade would be less than before. With the cycle
ergometer, weight loss does not have as great an effect on
physiological response to a standardized power output. Thus,
walking or running is often referred to as weight-dependent exercise,
while cycling is weight independent.
Cycle ergometers also have disadvantages. If the subject does
not regularly engage in that form of exercise, the leg muscles will
likely fatigue early in the exercise bout. This may prevent a subject
from attaining a true maximal intensity. When exercise is limited in
this way, responses are often referred to as peak exercise intensity
rather than maximal exercise intensity. This limitation may be
attributable to local leg fatigue, blood pooling in the legs (less blood
returns to the heart), or the use of a smaller muscle mass during
cycling than during treadmill exercise. Trained cyclists, however,
tend to achieve their highest peak values on the cycle ergometer.
Other Ergometers
Other ergometers allow athletes who compete in specific sports or
events to be tested in a manner that more closely approximates their
training and competition. For example, an arm ergometer may be
used to test athletes or nonathletes who use primarily their arms and
shoulders in physical activity. Arm ergometry has also been used
extensively to test and train athletes paralyzed below arm level. The
rowing ergometer was devised to test competitive rowers.
Valuable research data have been obtained by instrumenting
swimmers and monitoring them during swimming in a pool. However,
the problems associated with turns and constant movement led to
the use of two devices—tethered swimming and swimming flumes.
In tethered swimming, the swimmer is attached to a harness
connected to a rope, a series of pulleys, and counterbalancing
weights and must swim against the pull of the apparatus to maintain
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a constant position in the pool. A swimming flume allows swimmers
to more closely simulate their natural swimming strokes. The
swimming flume operates by pumps that circulate water past the
swimmer, who attempts to maintain body position in the flume. The
pump circulation can be increased or decreased to vary the speed at
which the swimmer must swim. The swimming flume, which
unfortunately is very expensive, has at least partially resolved the
problems with tethered swimming and has created new opportunities
to investigate the sport of swimming.
When one is choosing an ergometer, the concept of specificity is
particularly important with highly trained athletes. The more specific
the ergometer is to the actual pattern of movement used by the
athlete in his or her sport, the more meaningful will be the test
results.
In Review
Treadmills generally produce higher peak values than other ergometers for
almost all assessed physiological variable, such as heart rate, ventilation, and
oxygen uptake.
Cycle ergometers are the most appropriate devices for evaluating changes in
submaximal physiological function before and after training in people whose
weights have changed. Unlike treadmill exercise, cycle ergometer intensity is
largely independent of body weight.
Research Designs
In exercise physiology research, there are two basic types of
research design: cross-sectional and longitudinal. With a crosssectional research design, a cross section of the population of
interest (that is, a representative sample) is tested at one specific
time, and the differences between subgroups from that sample are
compared. With a longitudinal research design, the same
research subjects are retested periodically after initial testing to
measure changes over time in variables of interest.
The differences between these two approaches are best
understood through an example. The objective of a research study is
to determine whether a regular program of distance running
increases the concentration of cardioprotective high-density
76
lipoprotein cholesterol (HDL-C) in the blood. High-density lipoprotein
cholesterol is the desirable form of cholesterol; increased
concentrations are associated with reduced risk for heart disease.
Using the cross-sectional approach, one could, for example, test a
large number of people who fall into the following categories:
A group of subjects who do no training (the control group)
A group of subjects who run 24 km (15 mi) per week
A group of subjects who run 48 km (30 mi) per week
A group of subjects who run 72 km (45 mi) per week
A group of subjects who run 96 km (60 mi) per week
One would then compare the results from all the groups, basing
one’s conclusions on how much running was done. Using this
approach, exercise scientists found that weekly running results in
elevated HDL-C levels, suggesting a positive health benefit related
to running distance. Furthermore, as illustrated in figure 0.14, there
was a dose–response relation between these variables—the
higher the dose of exercise training, the higher the resulting
concentration of HDL-C. It is important to remember, however, that
with a cross-sectional design, these are different groups of runners,
not the same runners at different training volumes.
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FIGURE 0.14 The relation between distance run per week and average high-density lipoprotein
cholesterol (HDL-C) concentrations across five groups: nontraining control (0 km/week), 24 km/week,
48 km/week, 72 km/week, and 96 km/week. This illustrates a cross-sectional study design.
Using the longitudinal approach to test the same question, one
could design a study in which untrained people would be recruited to
participate in a 12-month distance-running program. One could, for
example, recruit 40 people willing to begin running and then
randomly assign 20 to a training group and the remaining 20 to a
control group. Both groups would be followed for 12 months. Blood
samples would be tested at the beginning of the study and then at 3month intervals, concluding at 12 months when the program ended.
With this design, both the running group and the control group would
be followed over the entire period of the study, and changes in their
78
HDL-C levels could be determined across each period. Studies have
been conducted using this longitudinal design to examine changes in
HDL-C with training, but their results have not been as clear as the
results of the cross-sectional studies. See figure 0.15 as an example.
Note that in this figure, in contrast to figure 0.14, there is only a small
increase in HDL-C in the subjects who are training. The control
group stays relatively stable, with only minor fluctuations in their
HDL-C from one 3-month period to the next.
A longitudinal research design is usually best suited to studying
changes in variables over time. Too many factors that may taint
results can influence cross-sectional designs. For example, genetic
factors might interact so that those who perform well in long-distance
running are also those who have high HDL-C levels. Also, different
populations might follow different diets. In a longitudinal study, diet
and other variables can be more easily controlled. However,
longitudinal studies are time consuming and expensive to conduct,
and are not always possible; cross-sectional studies do provide
some insight into the questions at hand.
FIGURE 0.15 The relation between months of distance-running training and average high-density
lipoprotein cholesterol (HDL-C) concentrations in an experimental group (20 subjects, distance training)
79
and a sedentary (20 subjects) control group. This illustrates a longitudinal study design.
Research Controls
When we conduct research, it is important to be as careful as
possible in designing the study and collecting the data. We see from
figure 0.15 that changes in a variable over time resulting from an
intervention such as exercise can be very small. Yet, even small
changes in a variable such as HDL-C can mean a substantial
reduction in risk for heart disease. Recognizing this, scientists design
studies aimed at providing results that are both accurate and
reproducible. This requires that studies be carefully controlled.
Research controls are applied at various levels. Starting with the
design of the research project, the scientist must determine how to
control for variation in the subjects used in the study. The scientist
must determine if it is important to control for the subjects’ sex, age,
or body size. To use age as an example, for certain variables, the
response to an exercise training program might be different for a
child or an aged person compared with a young or middle-aged
adult. Is it important to control for the subject’s smoking or dietary
status? Considerable thought and discussion are needed to make
sure that the subjects used in a study are appropriate for the specific
research question being asked.
For almost all studies, it is critical to have a control group. In the
longitudinal research design for the cholesterol study described
earlier, the control group acts as a comparison group to make
certain that any changes observed in the running group are
attributable solely to the training program and not to any other
factors, such as the time of the year or aging of the subjects during
the course of the study. Experimental designs often employ a
placebo group. Thus, in a study in which a subject might expect to
have a benefit from the proposed intervention, such as the use of a
specific food or drug, a scientist might decide to use three groups of
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subjects: an intervention group that receives the actual food or drug,
a placebo group that receives an inert substance that looks exactly
like the actual food or drug, and a control group that receives
nothing. (The last group often serves as a time control, accounting
for nonexperimentally induced changes that may occur over the
course of the study period.) If the intervention and placebo groups
improve their performance to the same level and the control group
does not improve performance, then the improvement is likely the
result of the placebo effect, or the expectation that the substance will
improve performance. If the intervention group improves
performance, and the placebo and control groups do not, then we
can conclude that the intervention does improve performance.
One other way of controlling for the placebo effect is to conduct a
study that uses a crossover design. In this case, each group
undergoes both treatment and control trials at different times. For
example, one group is administered the intervention for the first half
of the study (e.g., 6 months of a 12-month study) and serves as a
control during the last half of the study. The second group serves as
a control during the first half of the study and receives the
intervention during the second half. In some cases, a placebo can be
used in the control phase of the study. Chapter 16, Ergogenic Aids in
Sport, provides further discussion of placebo groups.
81
It is equally important to control data collection. The equipment
must be calibrated so the researcher knows that the values
generated by a given piece of equipment are accurate, and the
procedures used in collecting data must be standardized. For
example, when using a scale to measure the weight of subjects,
researchers need to calibrate that scale by using a set of calibrated
weights (e.g., 10 kg, 20 kg, 30 kg, and 40 kg) that have been
measured on a precision scale. These weights are placed on the
scale to be used in the study, individually and in combination, at least
once a week to provide certainty that the scale is measuring the
weights accurately. As another example, electronic analyzers used
to measure respiratory gases need to be calibrated frequently with
82
gases of known concentration to ensure the accuracy of these
analyses.
Finally, it is important to know that all test results are reproducible.
In the example illustrated in figure 0.15, the HDL-C of an individual is
measured every 3 months. If that person is tested 5 days in a row
before he or she starts the training program, one would expect the
HDL-C results to be similar across all 5 days, provided that diet,
exercise, sleep, and time of day for testing remained the same. In
figure 0.15, the values for the control group across 12 months varied
from about 44 to 45 mg/dl, whereas the exercise group values
increased from 45 to 47 mg/dl. Over five consecutive days, the
measurements should not vary by more than 1 mg/dl for any one
person if the researcher is going to pick up this small change over
time. To control for reproducibility of results, scientists generally take
several measurements, sometimes on different days, and then
average the results before, during, and at the end of an intervention.
Confounding Factors in Exercise Research
Many factors can alter the body’s acute response to a bout of
exercise. For example, environmental conditions such as the
temperature and humidity of the laboratory and the amount of light
and noise in the test area can markedly affect physiological
responses, both at rest and during exercise. Even the timing,
volume, and content of the last meal and the quantity and quality of
sleep the night before must be carefully controlled in research
studies.
To illustrate this, table 0.1 shows how varying environmental and
behavioral factors can alter heart rate at rest and during running on a
treadmill at 14 km/h (9 mph). The subject’s heart rate response
during exercise differed by 25 beats/min when the air temperature
was increased from 21 °C (70 °F) to 35 °C (95 °F). Most
physiological variables that are normally measured during exercise
are similarly influenced by environmental fluctuations. Whether one
is comparing a person’s exercise results from one day to another or
comparing the responses of two different subjects, all of these
factors must be controlled as carefully as possible.
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Physiological responses, both at rest and during exercise, also
vary throughout the day. The term diurnal variation refers to
fluctuations that occur during a 24 h day. Because such variables as
body temperature and heart rate vary naturally during a 24 h period,
testing the same person in the morning on one day and in the
afternoon on the next will produce different results. Test times must
be standardized to control for this diurnal effect.
TABLE 0.1 Heart Rate Responses to Running Differ with
Variations in Environmental and Behavioral Conditions
Heart rate (beats/min)
Environmental and behavioral factors
Temperature (at 50% humidity)
21 °C (70 °F)
35 °C (95 °F)
Humidity (at 21 °C)
50%
90%
Noise level (at 21 °C, 50% humidity)
Low
High
Food intake (at 21 °C, 50% humidity)
Small meal 3 h before exercising
Large meal 30 min before exercising
Sleep (at 21 °C, 50% humidity)
8 h or more
6 h or less
Rest
Exercise
60
70
165
190
60
65
165
175
60
70
165
165
60
70
165
175
60
65
165
175
At least one other physiological cycle must also be considered.
The normal 28-day menstrual cycle often involves considerable
variations in
body weight,
total body water and blood volume,
body temperature,
metabolic rate, and
heart rate and stroke volume (the amount of blood leaving
the heart with each contraction).
Exercise scientists must control for menstrual cycle phase or the use
of oral contraceptives (which similarly alter hormonal status), or both,
when testing women. When older women are being tested, testing
strategies must take into account menopause and hormone
replacement therapies.
84
In summary, the conditions under which research participants are
monitored, at rest and during exercise, must be carefully controlled.
Environmental factors, such as temperature, humidity, altitude, and
noise, can affect the magnitude of response of all basic physiological
systems, as can behavioral factors such as eating patterns and
sleep. Likewise, physiological measurements must be well controlled
for diurnal and menstrual cycle variations.
Units and Scientific Notation
A set of international standards for units and abbreviations (SI, Le
Système International d’Unités) serves as the preferred units of
measurement in exercise and sport physiology. In this text, alternate
units in common use (such as weight in pounds) are often provided
as well. Many of these units are provided on the inside front cover of
this text, and conversions for units in common use are found on the
inside back cover.
In common writing and even in mathematics, the ratio between
two numbers is typically written using a slash (/). For example, in dry
air at 20 °C, the speed of sound is 343 m/s. That notation works well
for simple fractions or ratios, and we have maintained it in this text.
However, the notation gets confusing for relations of several—that is,
more than two—variables. Take, for instance, one of the cornerstone
measurements in exercise physiology, an individual’s maximal
oxygen uptake or maximal aerobic capacity, abbreviated O2max.
This important physiological measurement is the maximal volume of
oxygen that an individual can use during exhaustive aerobic
exercise, and can be measured in liters per minute, or L/min.
However, because a large person can use more oxygen yet not be
more aerobically fit, we often standardize this value to body weight in
kilograms, that is, milliliters per kilogram per minute. Now the
notation becomes a bit more complex and potentially more
confusing. We could write the units as ml/kg/min, but what is being
divided by what in this notation? Recall that L/min can also be written
as L · min−1, just as the fraction 1/4 = 1 · 4−1. To avoid errors and
ambiguity, in exercise physiology, we use the exponent notation any
time more than two variables are involved. Therefore, milliliters per
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kilogram per minute is written as ml · kg−1 · min−1 rather than
ml/kg/min.
Reading and Interpreting Tables and Graphs
This book contains references to specific research studies that have
had a major impact on our understanding of exercise and sport
physiology. Once scientists complete a research project, they submit
the results of their research to one of the many research journals in
sport and exercise physiology.
As in other areas of science, most of the quantitative research in
exercise physiology is presented in the form of tables and graphs.
Tables and graphs provide an efficient way for researchers to
communicate the results of their studies to other scientists. For the
student in exercise and sport physiology, a working knowledge of
how to read and interpret tables and graphs is critical.
Tables are usually used to convey a large number of data points
or complex data that are affected by several factors. Take table 0.1
as an example. It is important to first look at the title of the table,
which identifies what information is being presented. In this case, the
table is designed to illustrate how various conditions affect heart
rate, at rest and during exercise. The left-hand column, along with
the horizontal subheadings (like “Humidity (at 21 °C)”), specify the
conditions under which the heart rate was measured. Columns 2 and
3 provide the mean heart rate values that correspond to each
condition, with the middle column giving the resting value and the
right-most column the exercise value. In every good table and graph,
the units for each variable are clearly presented; in this table, heart
rate is expressed in beats/min, or beats per minute. Pay careful
attention to the units of measure used when interpreting a table or
graph. From this table—a relatively simple one—we see that both
resting and exercise heart rate were increased by increased ambient
temperature and humidity, while noise level affected only resting
heart rate. Similarly, consuming a large meal or getting less than 6 h
of sleep also raises heart rate. These data could not easily have
been shown in graphical form.
Graphs can provide a better view of trends in data, response
patterns, and comparisons of data collected from two or more groups
86
of subjects. For some students, graphs can be more difficult to read
and interpret, but graphs are, and will remain, a critical tool in the
understanding of exercise physiology. First, every graph has a
horizontal axis, or x-axis, for the independent variable and a
vertical axis, or y-axis, (or sometimes two) for the dependent
variable or variables. Independent variables are those factors that
are manipulated or controlled by the researcher, while dependent
variables are those that change with—that is, depend on—the
independent variables.
In figure 0.16, time of day is the independent variable and is
therefore placed along the x-axis of the graph, while heart rate is the
dependent variable (since heart rate depends on the time of day)
and is therefore plotted on the y-axis. The units of measure for each
variable are clearly displayed on the graph. Figure 0.16 is in the form
of a line graph. Line graphs are useful in illustrating patterns or
trends in data but should be used only to compare two variables that
change in a continuous manner (for example, across time) and only
if both the dependent and independent variables are numbers.
In a line graph, if the dependent variable goes up or down at a
constant rate with the independent variable, the result will be a
straight line. However, in physiology, the response pattern between
variables is often not a straight line but a curve of one shape or
another. In such cases, pay close attention to the slope of various
parts of the curve as it changes across the graph. For instance,
figure 0.17 shows the concentration of lactate in the blood as
subjects walk-run on a treadmill at various increasing speeds. At low
treadmill speeds of 4 to 8 km/h, lactate increases very little.
However, at about 8.5 km/h, a threshold is reached beyond which
lactate increases more dramatically. In many physiological
responses, both the threshold (onset of response) and the slope of
the response beyond that threshold are important.
Data can also be plotted in the format of a bar graph. Bar graphs
are commonly used when only the dependent variable is a number
and the independent variable is a category. Bar graphs often show
treatment effects, as in figure 0.14, which was previously discussed.
Figure 0.14 shows the effect of distance run per week (a category)
on HDL-C (a numerical response) in the bar graph format.
87
FIGURE 0.16 This line graph depicts the relation between the time of day (on the x-axis, independent
variable) and heart rate during low-intensity exercise (on the y-axis, dependent variable) that was
measured at that time of day with no change in the exercise intensity.
88
FIGURE 0.17 A line graph showing the nonlinear nature of many physiological responses. This graph
shows that above a threshold (onset of response) of about 8.5 km/h, the slope of the blood lactate
response increases sharply.
In Review
Exercise physiologists make use of both cross-sectional (finding differences
between groups at one point in time) and longitudinal (retesting the same
subjects at different points in time) research designs.
For all sound research studies, it is critical to have a control group as well as an
experimental group. The control group often involves a placebo treatment rather
than no treatment at all.
Exercise physiologists use the SI units of measurement and abbreviations.
89
IN CLOSING
In this introduction, we highlighted the historical roots and scientific
underpinnings of exercise and sport physiology. We learned that the current
state of knowledge in these fields builds on the past and is a bridge to the
future—many questions remain unanswered. New and exciting approaches
and techniques are being developed continually. While reductionist (e.g.,
genomics) approaches are growing in popularity, being able to integrate those
findings into a systems and whole-body perspective will never go out of style.
Exercise and sport physiology is an important part of integrative and
translational physiology. We briefly defined the acute responses to exercise
bouts and chronic adaptations to long-term training. We concluded with an
overview of the principles used in sport and exercise physiology research as
well as an introduction to interpreting graphs, some important terminology, and
SI units and their notation.
In part I, we begin examining physical activity the way exercise
physiologists do as we explore the essentials of movement. In the next chapter,
we examine the structure and function of skeletal muscle, how it produces
movement, and how it responds during exercise.
KEY TERMS
acute exercise
bioinformatics
chronic adaptation
control group
crossover design
cross-sectional research design
cycle ergometer
dependent variable
diurnal variation
dose–response relation
environmental physiology
epigenetics
ergometer
exercise physiology
genomics
genotype
homeostasis
independent variable
integrative physiology
longitudinal research design
90
phenotype
physiology
placebo group
sport physiology
training effect
translational physiology
treadmill
STUDY QUESTIONS
1.
2.
What is exercise physiology? How does sport physiology differ?
3.
Describe what is meant by “studying chronic adaptations to exercise
training.”
4.
Describe the evolution of exercise physiology from the early studies of
anatomy. Who were some of the key figures in the development of this
field?
5.
Describe the founding and the key areas of research emphasized by the
Harvard Fatigue Laboratory. Who was the first research director of this
laboratory?
6.
Name the three Scandinavian physiologists who conducted research in the
Harvard Fatigue Laboratory.
7.
What is an ergometer? Name the two most commonly used ergometers
and explain their advantages and disadvantages.
8.
What factors must researchers consider when designing a research study
to ensure that they get accurate and reproducible results?
Provide an example of “studying acute responses to a single bout of
exercise.”
9.
10.
What is translational physiology?
11.
List several environmental conditions that could affect one’s response to
an acute bout of exercise.
12.
What are the advantages and disadvantages of a cross-sectional versus a
longitudinal study design?
13.
When should data be depicted as a bar graph as opposed to a line graph?
What purpose does a line graph serve?
Define the following terms and discuss their relevance to exercise
physiology: genomics, epigenetics, bioinformatics, genotype, and
phenotype.
91
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter
QUIZ tests your understanding of the material covered in the chapter.
92
PART I
Exercising Muscle
In the introduction, we explored the foundations of exercise and
sport physiology. We defined these fields of study, gained a historical
perspective of their development, looked at present trends as well as
the future of exercise physiology, and established some basic
concepts that we will follow through the remainder of this book. We
also examined the tools and research methods used by exercise
physiologists along with some tips about interpreting graphs and
scientific notation. With this foundation, we can begin our main
objective—understanding how the human body performs, and
adapts to, exercise and physical activity. Because muscle is the
foundation of all movement, we start with chapter 1, Structure and
Function of Exercising Muscle, where we focus on skeletal muscle,
examining the structure and function of skeletal muscles and muscle
fibers and how they contract. We learn how muscle fiber types differ
and why these differences are important to specific types of activity.
Because movement requires energy, in chapter 2, Fuel for Exercise:
Bioenergetics and Muscle Metabolism, we study the principles of
metabolism, focusing on the primary form of usable energy,
adenosine triphosphate (ATP), and how it is provided from the foods
that we eat through three energy systems. In chapter 3, Neural
Control of Exercising Muscle, we discuss how the nervous system
initiates and controls muscle actions. Chapter 4, Hormonal Control
During Exercise, presents an overview of the complex endocrine
system, with a focus on hormonal control of energy metabolism,
body fluid and electrolyte balance during exercise, and caloric intake.
Finally, chapter 5, Energy Expenditure, Fatigue, and Muscle
93
Soreness, discusses the measurement of energy expenditure, how
energy expenditure changes from rest to varying types and
intensities of exercise, the various causes of fatigue that limits
exercise performance, and the causes of muscle cramping and
feelings of soreness.
94
95
1
Structure and Function of Exercising
Muscle
In this chapter and in the web study guide
Anatomy of Skeletal Muscle
Muscle Fibers
Myofibrils
AUDIO FOR FIGURE 1.2 describes the structures of a muscle.
ACTIVITY 1.1 Muscle Structure reviews the basic structures of muscle.
AUDIO FOR FIGURE 1.3 describes the structure of a muscle fiber.
ACTIVITY 1.2 Structure of a Skeletal Muscle Cell reviews the structures in a single muscle fiber.
AUDIO FOR FIGURE 1.5 describes the structure of a sarcomere.
ACTIVITY 1.3 Structure of the Sarcomere reviews the structures in a sarcomere.
Muscle Fiber Contraction
Excitation–Contraction Coupling
Role of Calcium in the Muscle Fiber
The Sliding Filament Theory: How Muscles Create Movement
Energy for Muscle Contraction
Muscle Relaxation
AUDIO FOR FIGURE 1.7 describes the structure of a motor unit.
ANIMATION FOR FIGURE 1.8 breaks down excitation–contraction coupling.
ACTIVITY 1.4 Sliding Filament Theory describes this theory of muscle contraction and explores what
happens at the cellular and gross motor movement levels.
ANIMATION FOR FIGURE 1.9 shows the function of a sarcomere during muscle contraction.
ANIMATION FOR FIGURE 1.10 shows the steps of the contractile cycle in a sarcomere.
Muscle Fiber Types
Characteristics of Type I and Type II Fibers
Distribution of Fiber Types
Fiber Type and Exercise
96
Determination of Fiber Type
AUDIO FOR FIGURE 1.11 describes the muscle fiber distinctions.
ACTIVITY 1.5 Fiber Types differentiates between type I and type II skeletal muscle fibers.
Skeletal Muscle and Exercise
Muscle Fiber Recruitment
Fiber Type and Athletic Success
Muscle Contraction
ACTIVITY 1.6 Fiber Recruitment tests your understanding of the types of muscle fibers recruited and the
order of recruitment.
ACTIVITY 1.7 Generation of Force reviews the factors that influence the development of muscle force.
AUDIO FOR FIGURE 1.14 describes the concepts of twitch, summation, and tetanus.
AUDIO FOR FIGURE 1.15 describes the variation in force with changes in sarcomere length.
AUDIO FOR FIGURE 1.16 explains the relationship between velocity and muscle force production.
In Closing
97
L
iam Hoekstra possesses a physique and physical attributes like many
professional athletes: ripped abdominal muscles, enough strength to perform feats
like an iron cross and inverted sit-ups, and amazing speed and agility. Not bad when
you consider the fact that Liam could do all this when he was just 19 months old and
weighed 10 kg (22 lb)! Liam has a rare genetic condition called myostatin-related
muscle hypertrophy, a condition that was first described in an abnormally muscular
breed of beef cattle in the late 1990s. Myostatin is a protein that inhibits the growth
of skeletal muscles; myostatin-related muscle hypertrophy is a genetic mutation that
blocks production of this inhibitory growth factor and thus promotes the rapid growth
and development of skeletal muscles.
Liam’s condition is extremely rare in humans, with fewer than 100 cases
documented worldwide. However, studying this genetic phenomenon has helped
scientists unlock secrets of how skeletal muscles grow and deteriorate. Research on
Liam’s condition could lead to new treatments for debilitating muscular conditions
such as muscular dystrophy. On the darker side, it could open up a whole new realm
of abuse by athletes who are looking for shortcuts to develop muscle size and
strength, not unlike the illicit and dangerous use of anabolic steroids.
When the heart beats, when partially digested food moves through
the intestines, and when the body moves in any way, muscle is
involved. These many and varied functions of the muscular system
are performed by three distinct types of muscle (see figure 1.1):
smooth muscle, cardiac muscle, and skeletal muscle.
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FIGURE 1.1 Microscopic photographs of the three types of muscle: (a) skeletal, (b) cardiac, and (c)
smooth.
Smooth muscle is sometimes called involuntary muscle because it
is not under direct conscious control. It is found in the walls of most
blood vessels, where its contraction or relaxation leads to vessel
constriction or dilation, respectively, to regulate blood flow. It is also
found in the walls of most internal organs, allowing them to contract
and relax, for example, to move food through the digestive tract, to
expel urine, or to give birth.
Cardiac muscle is found only in the heart, composing the vast
majority of the heart’s structure. It shares some characteristics with
skeletal muscle, but like smooth muscle, it is not under conscious
control. Cardiac muscle in essence controls itself, with some fine-
99
tuning by the nervous and endocrine systems. Cardiac muscle is
discussed more fully in chapter 6.
Skeletal muscles are under conscious control and are so named
because most attach to and move the skeleton. Together with the
bones of the skeleton, they make up the musculoskeletal system.
The names of many of these muscles have found their way into our
everyday vocabulary—such as deltoids, pectorals (or “pecs”), and
biceps—but the human body contains more than 600 skeletal
muscles. The thumb alone is controlled by nine separate muscles!
Exercise requires movement of the body, which is accomplished
through the action of skeletal muscles. Because exercise and sport
physiology depend on human movement, the primary focus of this
chapter is on the structure and function of skeletal muscle. Although
the anatomical structures and control of smooth, cardiac, and skeletal
muscle differ in many respects, their principles of action—for
example, creating tension, shortening, and lengthening—are similar.
Anatomy of Skeletal Muscle
When we think of muscles, we visualize each muscle as a single unit.
This is natural because a skeletal muscle most often acts as a single
entity. But skeletal muscles are far more complex than that.
If a person were to dissect a muscle, he or she would first cut
through an outer connective tissue covering known as the
epimysium (see figure 1.2). It surrounds the entire muscle and
functions to hold it together and give it shape. Once through the
epimysium, one would see small bundles of fibers wrapped in a
connective tissue sheath. These bundles are called fascicles (or
fasciculi), and the connective tissue sheath surrounding each
fascicle is the perimysium.
Finally, by cutting through the perimysium and using a microscope,
one would see the individual muscle fibers, each of which is a
muscle cell. Unlike most cells in the body, which have a single
nucleus, muscle cells are multinucleated. A sheath of connective
tissue, called the endomysium, also covers each muscle fiber. It is
generally thought that muscle fibers extend from one end of the
muscle to the other, but under the microscope, muscle bellies (the
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thick middle parts of muscles) often divide into compartments or more
transverse fibrous bands (inscriptions).
Because of this compartmentalization, the longest human muscle
fibers are about 12 cm (4.7 in.), which corresponds to about 500,000
sarcomeres, the basic functional unit of the myofibril. The number of
fibers in different muscles ranges from several hundred (e.g., in the
tensor tympani, attached to the eardrum) to more than a million (e.g.,
in the medial gastrocnemius muscle).12
Muscle Fibers
Muscle fibers range in diameter from 10 to 120 μm, so they are nearly
invisible to the naked eye. The following sections describe the
structure of the individual muscle fiber.
FIGURE 1.2 The basic structure of muscle.
Plasmalemma
Looking closely at an individual muscle fiber, it is surrounded by a
plasma membrane, called the plasmalemma (figure 1.3). The
plasmalemma is part of a larger unit referred to as the sarcolemma.
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The sarcolemma is composed of the plasmalemma and the
basement membrane. (Some textbooks use the term sarcolemma to
refer to just the plasmalemma.12) At the end of each muscle fiber, its
plasmalemma fuses with the tendon, which inserts into the bone.
Tendons are made of fibrous cords of connective tissue that transmit
the force generated by muscle fibers to the bones, thereby creating
motion. So typically, individual muscle fibers are ultimately attached to
bone via the tendon.
RESEARCH PERSPECTIVE 1.1
Muscle Changes After Only 6 Weeks of Training
Architectural characteristics of a muscle, such as its thickness, pennation
angle (the angle at which the fibers are oriented within the muscle), and
fascicle length, all contribute to its ability to produce force. Changes in
structural characteristics have been demonstrated in many muscles in
response to mechanical stimuli, including long-term exercise training.
Understanding how—and how quickly—muscle architecture adapts to
exercise training is important for recreational exercisers beginning a training
program and athletes getting ready for competition.
A group of investigators recently used ultrasound imaging to examine the
architectural adaptations of the biceps femoris in a group of young men before
and after 6 weeks of either concentric or eccentric strength training.17
Eccentric strength training increased muscle fascicle length and reduced
pennation angle (the fascicles aligned better with the direction of the muscle).
In contrast, concentric strength training reduced fascicle length and increased
pennation angle (fascicles were angled more away from the full muscle’s
direction). After 4 weeks of detraining, eccentric training-induced alterations
were reversed, but the adaptations in response to concentric training were
maintained. Thus, short-term resistance training can cause structural
adaptations in the biceps that are highly specific to the mode of training.
Understanding architectural alterations that occur in response to training is
important for injury prevention and development of proper rehabilitation
programs.
102
FIGURE 1.3 The structure of a single muscle fiber.
The plasmalemma has several unique features that are critical to
muscle fiber function. It appears as a series of shallow folds along the
surface of the fiber when the fiber is contracted or in a resting state,
but these folds disappear when the fiber is stretched. This folding
allows stretching of the muscle fiber without disrupting the
plasmalemma. The plasmalemma also has junctional folds in the
innervation zone at the motor end plate, which assists in the
transmission of the action potential from the motor neuron to the
muscle fiber, as discussed later in this chapter. Finally, the
plasmalemma helps to maintain acid–base balance and transport of
metabolites from the capillary blood into the muscle fiber.12
Satellite cells are located between the plasmalemma and the
basement membrane. These cells are involved in the growth and
development of skeletal muscle and in muscle’s adaptation to injury,
immobilization, and training. This is discussed in greater detail in
subsequent chapters.
Sarcoplasm
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Inside the plasmalemma, a muscle fiber contains successively
smaller subunits, as shown in figure 1.3. The largest of these are
myofibrils, the contractile element of the muscle, which are described
later. A gelatin-like substance fills the spaces within and between the
myofibrils. This is the sarcoplasm. It is the fluid part of the muscle
fiber—its cytoplasm. The sarcoplasm contains mainly dissolved
proteins, minerals, glycogen, fats, and necessary organelles. It differs
from the cytoplasm of most cells because it contains a large quantity
of stored glycogen as well as the oxygen-binding compound
myoglobin, which is similar in structure and function to the
hemoglobin found in red blood cells.
The sarcoplasm also houses an extensive network
of transverse tubules (T-tubules), which are extensions of the
plasmalemma that pass laterally through the muscle fiber. These
tubules are interconnected as they pass among the myofibrils,
allowing nerve impulses received by the plasmalemma to be
transmitted rapidly to individual myofibrils. The tubules also provide
pathways from outside the fiber to its interior, enabling substances to
enter the cell and waste products to leave the fibers.
Transverse Tubules
A longitudinal network of tubules, known as the
sarcoplasmic reticulum (SR), is also found within the muscle fiber.
These membranous channels parallel the myofibrils and loop around
them. The SR serves as a storage site for calcium, which is essential
for muscle contraction. Figure 1.3 depicts the T-tubules and the SR.
Their functions are discussed in more detail later in this chapter when
we consider the process of muscle contraction.
Sarcoplasmic Reticulum
Myofibrils
Each muscle fiber contains several hundred to several thousand
myofibrils. These small fibers are made up of the basic contractile
elements of skeletal muscle—the sarcomeres. Under the electron
microscope, myofibrils appear as long strands of sarcomeres.
Sarcomeres
Under a light microscope, skeletal muscle fibers have a distinctive
striped appearance. Because of these markings, or striations, skeletal
104
muscle is also called striated muscle. This striation pattern is also
seen in cardiac muscle, so it too can be considered striated muscle.
Refer to figure 1.4, showing myofibrils within a single muscle fiber,
and note the striations. Note that dark regions, known as A-bands,
alternate with light regions, known as I-bands. Each dark A-band has
a lighter region in its center, the H-zone, which is visible only when
the myofibril is relaxed. There is a dark line in the middle of the Hzone called the M-line. The light I-bands are interrupted by a dark
stripe referred to as the Z-disk, also known as the Z-line.
FIGURE 1.4 An electron micrograph of myofibrils within a muscle fiber showing mitochondria (green)
between the myofibrils.
A sarcomere is the basic functional unit of a myofibril and the
basic contractile unit of muscle. Each myofibril is composed of
numerous sarcomeres joined end to end at the Z-disks. Each
sarcomere includes several elements found between each pair of Zdisks, in this sequence:
An I-band (light zone)
An A-band (dark zone)
An H-zone (in the middle of the A-band)
An M-line in the middle of the H-zone
The rest of the A-band
A second I-band
105
In Review
An individual muscle cell is called a muscle fiber.
Muscle fibers have a cell membrane and the same organelles—mitochondria,
lysosomes, and so on—as other cell types but are uniquely multinucleated.
A muscle fiber is enclosed by a plasma membrane called the plasmalemma.
The cytoplasm of a muscle fiber is called the sarcoplasm.
The extensive tubule network found in the sarcoplasm includes T-tubules, which
allow communication and transport of substances throughout the muscle fiber,
and the SR, which stores calcium.
The sarcomere is the smallest functional unit of a muscle.
Looking at individual myofibrils through an electron microscope,
one can differentiate two types of small protein filaments that are
responsible for muscle contraction. The thinner filaments are
composed primarily of actin, and the thicker filaments are primarily
myosin. The striations seen in muscle fibers result from the
alignment of these filaments, as illustrated in figure 1.4. The light Iband indicates the region of the sarcomere where there are only thin
filaments. The dark A-band represents the regions that contain both
thick and thin filaments. The H-zone is the central portion of the Aband and contains only thick filaments. The absence of thin filaments
causes the H-zone to appear lighter than the adjacent A-band. In the
center of the H-zone is the M-line, which is composed of proteins that
serve as the attachment site for the thick filaments and assist in
stabilizing the structure of the sarcomere. Z-disks, composed of
proteins, appear at each end of the sarcomere. Along with two
additional proteins, titin and nebulin, they provide points of
attachment and stability for the thin filaments.
Thick Filaments
About two-thirds of all skeletal muscle protein is myosin, the principal
protein of the thick filament. Each myosin filament typically contains
about 200 myosin molecules.
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FIGURE 1.5 The sarcomere contains a specialized arrangement of actin (thin) and myosin (thick)
filaments. The role of titin is to position the myosin filament to maintain equal spacing between the actin
filaments. Nebulin is often referred to as an anchoring protein because it provides a framework that
helps stabilize the position of actin.
Each myosin molecule is composed of two protein strands twisted
together (see figure 1.5). One end of each strand is folded into a
globular head, called the myosin head. Each thick filament contains
many such heads, which protrude from the thick filament to form
107
cross-bridges that interact during muscle contraction with specialized
active sites on the thin filaments. There is an array of fine filaments,
composed of titin, that stabilize the myosin filaments along their
longitudinal axis (see figure 1.5). Titin filaments extend from the Zdisk to the M-line.
Thin Filaments
Each thin filament, although often referred to simply as an actin
filament, is actually composed of three different protein molecules—
actin, tropomyosin, and troponin. Each thin filament has one end
inserted into a Z-disk, with the opposite end extending toward the
center of the sarcomere, lying in the space between the thick
filaments. Nebulin, an anchoring protein for actin, coextends with
actin and appears to play a regulatory role in mediating actin and
myosin interactions (figure 1.5). Each thin filament contains active
sites to which myosin heads can bind.
Actin forms the backbone of the filament. Individual actin
molecules are globular proteins (G-actin) and join together to form
strands of actin molecules. Two strands then twist into a helical
pattern, much like two strands of pearls twisted together.
Tropomyosin is a tube-shaped protein that twists around the actin
strands. Troponin is a more complex protein that is attached at
regular intervals to both the actin strands and the tropomyosin. This
arrangement is depicted in figure 1.5. Tropomyosin and troponin work
together in an intricate manner along with calcium ions to maintain
relaxation or initiate contraction of the myofibril, which we discuss
later in this chapter.
Titin: The Third Myofilament
Titin was not discovered until the late 1970s, well after the sliding
filament theory of muscle contraction was proposed. The sliding
filament theory adequately describes most functions of muscle during
shortening (concentric) and constant-length (isometric) contractions.
However, traditional cross-bridge theory does not explain why
muscles behave as if they have an internal spring—that is, they
produce greater force when stretched (eccentric contractions), a
mechanism sometimes called passive force enhancement.9 Recent
research has determined that titin’s stiffness increases with muscle
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activation and force development, acting like a spring in active
muscle.9,14,18
Titin extends from the Z-disk to the M-band in the sarcomere
(figure 1.5). It is attached to the myosin filament in the A-band region,
but extends freely in the I-band region, where it functions as a spring.
Titin has been known for decades to have structural functions, like
keeping myosin aligned during contraction and stabilizing adjacent
sarcomeres (figure 1.6). However, it is now known that when skeletal
muscles are activated by the release of calcium ions (Ca2+), some
calcium binds to titin, changing its stiffness. This helps explain why a
muscle’s ability to generate more force when stretched is not
accounted for by traditional actin–myosin cross-bridge theory.
Further, more recently, when titin is included in three-dimensional
models of the sarcomere as a third filament, it becomes clear that
filaments do not simply slide but actually twist with each cross-bridge
interaction. This has led to a new theory called the winding filament
theory that better explains how titin contributes to the force produced
by muscle sarcomeres at different lengths.15 In this updated theory,
titin is activated by the calcium ion influx and then winds around the
thin filaments, rotating them in the process.
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The role of titin in regulating skeletal muscle contractile force helps
explain the large increase in force that is observed when muscles are
actively stretched. That is, titin is increasingly recognized as a third
myofilament that is actively involved in the regulation of skeletal
muscle force generation. Among its roles are (1) stabilizing
sarcomeres and centering myosin filaments in the middle of the
sarcomere, (2) providing increased force when muscles are
stretched, and (3) preventing overstretching and damage to the
sarcomere by resisting active stretching.9
110
FIGURE 1.6 The mechanism through which the molecule titin acts during muscle contraction. Titin acts
as a spring element to increase the force generated and resists overstretch to prevent sarcomere
damage.
In Review
Myofibrils are composed of sarcomeres, the basic contractile units of a muscle.
A sarcomere is composed of two different-sized filaments, thick and thin filaments,
which are responsible for muscle contraction.
Myosin, the primary protein of the thick filament, is composed of two protein
strands, each folded into a globular head at one end.
The thin filament is composed of actin, tropomyosin, and troponin. One end of
each thin filament is attached to a Z-disk.
A third microfilament, titin, helps stabilize sarcomeres, provides increased force
when muscles are stretched, and prevents overstretching and damage to the
sarcomere.
Muscle Fiber Contraction
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The initiation of contraction of a skeletal muscle occurs in response to
a signal from the nervous system. An α-motor neuron is a nerve cell
that connects with and innervates many muscle fibers. A single αmotor neuron and all the muscle fibers it directly signals are
collectively termed a motor unit (see figure 1.7). The synapse or gap
between the α-motor neuron and a muscle fiber is referred to as a
neuromuscular junction. This is where communication between the
nervous and muscular systems occurs.
Excitation–Contraction Coupling
The complex sequence of events that triggers a muscle fiber to
contract is termed excitation–contraction coupling because it
begins with the excitation of a motor nerve and results in contraction
of the muscle fibers. The process, depicted in figure 1.8, is initiated
by a nerve impulse, or action potential, from the brain or spinal cord
to an α-motor neuron. The action potential arrives at the α-motor
neuron’s dendrites, specialized receptors on the neuron’s cell body.
From here, the action potential travels down the axon to the axon
terminals, which are located very close to the plasmalemma.
RESEARCH PERSPECTIVE 1.2
Curving Muscle Fascicles
Muscle fascicles are often drawn in a straight line for ease of illustration. Past
experimental measures of muscle fascicle characteristics were based on the
idea that the muscle fascicles were straight. However, within the muscle, they
are actually curved structures, and the curvature of the fascicles is now
recognized as an important characteristic relative to muscle function. Twodimensional (2D) modeling studies demonstrate that muscle fascicles take on
a curved path to provide mechanical stability within the muscle, particularly
during contraction. Muscle fascicles curve around regions of the muscle that
generate high pressures; thus, they curve more where the largest contractions
occur. These 2D models also hint that the curvature could extend into three
dimensions (3D), but, until recently, this possibility had not been examined
during active muscle contraction.
Using sophisticated imaging techniques, researchers have recently
quantified 3D fascicle curvature in triceps surae muscles during contractions
at different muscle lengths and torques.16 Fascicle curvatures increased as
the muscle contracted more, indicating an increase in intramuscular pressure
at greater levels of contraction. Because this study utilized new 3D imaging
approaches, the researchers were able to identify details about the fascicle
112
curvature that were not detectable in 2D. This more detailed and precise
interpretation of the noted 3D fascicle curvature parameters aids our
understanding of how pressure is developed in the contracting muscle and of
overall muscle function.
FIGURE 1.7 A motor unit includes one
α-motor neuron and all of the muscle fibers it innervates.
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When the action potential arrives at the axon terminals, these
nerve endings release a signaling molecule or neurotransmitter called
acetylcholine (ACh), which crosses the synaptic cleft and binds to
receptors on the plasmalemma (see figure 1.8a). If enough ACh
binds to the receptors, the action potential will be transmitted the full
length of the muscle fiber as ion gates open in the muscle cell
membrane and allow sodium to enter. This process is referred to as
depolarization. An action potential must be generated in the muscle
cell before the muscle cell can act. These neural events are
discussed more fully in chapter 3.
Role of Calcium in the Muscle Fiber
In addition to depolarizing the fiber membrane, the action potential
travels over the fiber’s network of tubules (T-tubules) to the interior of
the cell. The arrival of an electrical charge causes the adjacent SR to
release large quantities of stored calcium ions (Ca2+) into the
sarcoplasm (see figure 1.8b).
In the resting state, tropomyosin molecules cover the myosinbinding sites on the actin molecules, preventing the binding of the
myosin heads. Once calcium ions are released from the SR, they
bind to the troponin on the actin molecules. Troponin, with its strong
affinity for calcium ions, is believed to then initiate the contraction
process by moving the tropomyosin molecules off the myosin-binding
sites on the actin molecules. This is shown in figure 1.8c. Because
tropomyosin normally covers the myosin-binding sites, it blocks the
attraction between the myosin cross-bridges and actin molecules.
However, once the tropomyosin has been lifted off the binding sites
by troponin and calcium, the myosin heads can attach to the binding
sites on the actin molecules.
114
FIGURE 1.8 The sequence of events leading to muscle action, known as excitation–contraction
coupling. (a) In response to an action potential, a motor neuron releases acetylcholine (ACh), which
crosses the synaptic cleft and binds to receptors on the plasmalemma. If enough ACh binds, an action
potential is generated in the muscle fiber. (b) The action potential triggers the release of calcium ions
(Ca2+) from the terminal cisternae of the sarcoplasmic reticulum into the sarcoplasm. (c) The Ca2+ binds
to troponin on the actin filament, and the troponin pulls tropomyosin off the active sites, allowing myosin
heads to attach to the actin filament.
The Sliding Filament Theory: How Muscles Create Movement
When muscle contracts, muscle fibers shorten. How do they shorten?
The explanation for this phenomenon is termed the sliding filament
theory. When the myosin cross-bridges are activated, they bind with
actin, resulting in a conformational change in the cross-bridge, which
causes the myosin head to tilt and to drag the thin filament toward the
center of the sarcomere (see figures 1.9 and 1.10). This tilting of the
head is referred to as the power stroke. The pulling of the thin
115
filament past the thick filament shortens the sarcomere and
generates force. When the fibers are not contracting, the myosin
head remains in contact with the actin molecule, but the molecular
bonding at the site is weakened or blocked by tropomyosin.
Immediately after the myosin head tilts, it breaks away from the
active site, rotates back to its original position, and attaches to a new
active site farther along the actin filament. Repeated attachments and
power strokes cause the filaments to slide past one another, giving
rise to the term sliding filament theory. This process continues until
the ends of the myosin filaments reach the Z-disks, or until the Ca2+ is
pumped back into the SR. During this sliding (contraction), the thin
filaments move toward the center of the sarcomere and protrude into
the H-zone, ultimately overlapping. When this occurs, the H-zone is
no longer visible.
Recall that the sarcomeres are joined end to end within a myofibril.
Because of this anatomical arrangement, as sarcomeres shorten, the
myofibril shortens, causing muscle fibers within a fascicle to shorten.
The end result of many such fibers shortening is an organized muscle
contraction.
FIGURE 1.9 A sarcomere in its relaxed (top) and contracted (bottom) state, illustrating the sliding of the
actin and myosin filaments with contraction.
116
In Review
The sequence of events that starts with a motor nerve impulse and results in
muscle contraction is called excitation–contraction coupling.
Muscle contraction is initiated by an α-motor neuron impulse or action potential.
The motor neuron releases ACh, which opens up ion gates in the muscle cell
membrane, allowing sodium to enter the muscle cell (depolarization). If the cell is
sufficiently depolarized, an action potential is generated and muscle contraction
occurs.
When an α-motor neuron is activated, all of the muscle fibers in its motor unit are
stimulated to contract.
The action potential travels along the plasmalemma, then moves through the Ttubule system, causing stored calcium ions to be released from the SR.
Calcium ions bind with troponin. Then troponin moves the tropomyosin molecules
off of the myosin-binding sites on the actin molecules, opening these sites to allow
the myosin heads to bind to them.
Once a strong binding state is established with actin, the myosin head tilts, pulling
the thin filament past the thick filament. The tilting of the myosin head is the power
stroke.
Energy is required for muscle contraction to occur. The myosin head binds to the
high-energy molecule ATP, and ATPase on the head splits ATP into ADP and Pi,
releasing energy to fuel the contraction.
The end of muscle contraction is signaled when neural activity ceases at the
neuromuscular junction. Calcium is actively pumped out of the sarcoplasm and
back into the SR for storage. Tropomyosin moves to cover active sites on actin
molecules, leading to relaxation between the myosin heads and the binding sites.
Like muscle contraction, muscle relaxation requires energy supplied by ATP.
117
FIGURE 1.10 The molecular events of a contractile cycle illustrating the changes in the myosin head
during various phases of the power stroke.
Energy for Muscle Contraction
Muscle contraction is an active process, meaning that it requires
energy. In addition to the binding site for actin, a myosin head
contains a binding site for the molecule adenosine triphosphate
(ATP). The myosin molecule must bind with ATP for muscle
contraction to occur because ATP supplies the needed energy.
The enzyme adenosine triphosphatase (ATPase), which is
located on the myosin head, splits the ATP to yield adenosine
118
diphosphate (ADP), inorganic phosphate (Pi), and energy. The energy
released from this breakdown of ATP is used to power the tilting of
the myosin head. Thus, ATP is the chemical source of energy for
muscle contraction. This process is discussed in much more detail in
chapter 2.
Muscle Relaxation
Muscle contraction continues as long as calcium is available in the
sarcoplasm. At the end of a muscle contraction, calcium is pumped
back into the SR, where it is stored until a new action potential arrives
at the muscle fiber membrane. Calcium is returned to the SR by an
active calcium-pumping system. This is another energy-demanding
process that also relies on ATP. Thus, energy is required for both the
contraction and relaxation phases.
When the calcium is pumped back into the SR, troponin and
tropomyosin return to the resting conformation. This blocks the linking
of the myosin cross-bridges and actin molecules and stops the use of
ATP. As a result, the thick and thin filaments return to their original
relaxed state.
Muscle Fiber Types
Not all muscle fibers are alike. A single skeletal muscle contains
fibers having different speeds of shortening and ability to generate
maximal force: type I (also called slow or slow-twitch) fibers and type
II (also called fast or fast-twitch) fibers. Type I fibers take
approximately 110 ms to reach peak tension when stimulated. Type II
fibers, on the other hand, can reach peak tension in about 50 ms.
While the terms slow twitch and fast twitch continue to be used,
scientists now prefer to use the terminology type I and type II, as is
the case in this textbook.
Although only one form of type I fiber has been identified, type II
fibers can be further classified. In humans, the two major forms of
type II fibers are fast-twitch type a (type IIa) and fast-twitch type x
(type IIx). Figure 1.11 is a micrograph of human muscle in which
thinly sliced (10 μm) cross sections of a muscle sample have been
chemically stained to differentiate the fiber types. The type I fibers are
stained black; type IIa fibers are unstained and appear white; and
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type IIx fibers appear gray. Although not apparent in this figure, a third
subtype of fast-twitch fibers has also been identified: type IIc.
FIGURE 1.11 A photomicrograph showing type I (black), type IIa (white), and type IIx (gray) muscle
fibers.
The differences in the type IIa, type IIx, and type IIc fibers are not
fully understood, but type IIa fibers are believed to be the most
frequently recruited. Only type I fibers are recruited more frequently
than type IIa fibers. Type IIc fibers are the least often used. On
average, most muscles are composed of roughly 50% type I fibers
and 25% type IIa fibers. The remaining 25% are mostly type IIx, with
type IIc fibers making up only 1% to 3% of the muscle. Because
knowledge about type IIc fibers is limited, we will not discuss them
further. The exact percentage of each of these fiber types varies
greatly in various muscles and among individuals, so the numbers
listed here are only averages. This extreme variation is most evident
in athletes, as we will see later in this chapter when we compare fiber
types in athletes across sports and events within sports.
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In the early 1900s, a needle biopsy procedure was developed to
study muscular dystrophy. In the 1960s, this technique was adapted
to sample muscle for studies in exercise physiology, specifically to
help determine muscle fiber types.
FIGURE 1.12 (a) The use of a biopsy needle to obtain a sample from the leg muscle of an elite female
runner. (b) A close-up view of a muscle biopsy needle and a small piece of muscle tissue.
A muscle biopsy (figure 1.12) involves removing a very small piece
of muscle tissue from the muscle belly for analysis. The area from
which the sample is taken is first numbed with a local anesthetic, and
then a small incision (approximately 1 cm, or 0.4 in.) is made with a
scalpel through the skin, subcutaneous tissue, and connective tissue.
A hollow needle is then inserted to the appropriate depth into the
belly of the muscle. A small plunger is pushed through the center of
the needle to snip off a very small sample of muscle. The biopsy
needle is withdrawn, and the sample, weighing 10 to 100 mg, is
removed, cleaned of blood, mounted, and quickly frozen. It is then
thinly sliced, stained, and examined under a microscope.
This method allows us to study muscle fibers and gauge the
effects of acute exercise and chronic training on fiber composition.
Microscopic and biochemical analyses of the samples aid our
understanding of the muscles’ ability to produce energy for
contraction.
Characteristics of Type I and Type II Fibers
Different muscle fiber types play different roles in exercise and sport.
This is largely due to differences in their inherent characteristics.
ATPase
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Type I and type II fibers differ in their speed of contraction. This
difference results primarily from different forms of myosin ATPase.
Recall that myosin ATPase is the enzyme that splits ATP to release
energy to drive contraction. Type I fibers have a slow form of myosin
ATPase, whereas type II fibers have a fast form. In response to
neural stimulation, ATP is split more rapidly in type II fibers than in
type I fibers. As a result, cross-bridges cycle more rapidly in type II
fibers.
One of the methods used to classify muscle fibers is a chemical
staining procedure applied to a thin slice of tissue. This staining
technique measures the ATPase activity in the fibers. Thus, the type
I, type IIa, and type IIx fibers stain differently, as depicted in figure
1.11. This technique makes it appear that each muscle fiber has only
one type of ATPase, but fibers can have a mixture of ATPase types.
Some have a predominance of type I ATPase, but others have mostly
type II ATPase. Their appearance in a stained slide preparation
should be viewed as a continuum rather than as absolutely distinct
types.
A newer method for identifying fiber types is to chemically separate
the different types of myosin molecules (isoforms) by using a process
called gel electrophoresis. In electrophoresis, the isoforms are
separated by weight in an electric field to show the bands of protein
(i.e., myosin) that characterize type I, type IIa, and type IIx fibers.
Although our discussion here categorizes fiber types simply as slow
twitch (type I) and fast twitch (type IIa and type IIx), scientists have
further subdivided these fiber types. The use of electrophoresis has
led to the detection of myosin hybrids or fibers that possess two or
more forms of myosin. With this method of analysis, the fibers are
classified as I, Ic (I/IIa), IIc (IIa/I), IIa, IIax, IIxa, and IIx.12 In this book,
we will use the histochemical method of identifying fibers by their
primary isoforms, types I, IIa, and IIx.
Table 1.1 summarizes the characteristics of the different muscle
fiber types. The table also includes alternative names that are used in
other classification systems to refer to the various muscle fiber types.
TABLE 1.1 Classification of Muscle Fiber Types
Fiber classification
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System 1 (preferred)
System 2
System 3
Type I
Slow twitch (ST)
Slow oxidative (SO)
Type IIa
Fast-twitch a (FTa)
Fast oxidative/glycolytic (FOG)
Type IIx
Fast-twitch x (FTx)
Fast glycolytic (FG)
Characteristics of fiber types
Oxidative capacity
Glycolytic capacity
Contractile speed
Fatigue resistance
Motor unit strength
High
Low
Slow
High
Low
Moderately high
High
Fast
Moderate
High
Low
Highest
Fast
Low
High
Sarcoplasmic Reticulum
Type II fibers have a more highly developed SR than do type I fibers.
Thus, type II fibers are more adept at delivering calcium into the
muscle cell when stimulated. This ability is thought to contribute to
the faster speed of contraction (Vo) of type II fibers. On average,
human type II fibers have a Vo that is five to six times faster than that
of type I fibers. Although the amount of force (Po) generated by type II
and type I fibers with the same diameter is about the same, the
calculated power (μN · fiber length−1 · s−1) of a type II fiber is three to
five times greater than that of a type I fiber because of a faster
shortening velocity. This may explain in part why individuals who have
a predominance of type II fibers in their leg muscles tend to be better
sprinters than individuals who have a high percentage of type I fibers,
all other things being equal.
RESEARCH PERSPECTIVE 1.3
More About Titin
Eccentric contractions are those during which active muscles are stretched or
elongated, such as during the lowering of a weight by the biceps or walking
down stairs. Unlike for concentric contractions, the classic theories of muscle
contraction—the sliding filament and cross-bridge theories—do not agree well
with some aspects of eccentrically contracting muscles. In the cross-bridge
model, greater force is developed during an eccentric contraction than for a
corresponding isometric or concentric contraction because the attached crossbridges are more strained. However, skeletal muscles are known to also have
history-dependent properties; that is, muscles behave differently depending on
preceding contractions. For example, when isometric contractions follow an
eccentric contraction, they often demonstrate a longer-lasting, steady-state
isometric force compared with the force produced during an isometric
contraction not preceded by an eccentric contraction. The classic cross-bridge
model involving actin and myosin does not explain such history-dependent
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properties of skeletal muscle, necessitating a careful reassessment of the
currently accepted theory of muscle contraction.
A group of researchers recently proposed a new mechanism that better
explains the history-dependent properties of muscle and eccentric
contractions by adding a small component to the classic cross-bridge theory.10
This tweak includes a new key role for the structural protein titin, whose
stiffness and force are adjusted upon activation and force production. In this
new model, muscle can be stretched passively against little resistance, but
upon activation, titin-based force becomes dominant and contributes to
eccentric force.
Titin’s traditional role (discussed in this chapter) has been associated with
centering the thick filaments in the sarcomere and preventing sarcomeres
from becoming overstretched by putting the brakes on active stretching. Yet
another function of titin is to serve as the third sarcomere myofilament,
contributing to active force production during and following eccentric
contractions. In this role, titin appears to be critical in the residual force
enhancement in skeletal muscle after an eccentric contraction. This theory is
based on research evidence that experimentally eliminating titin in single
myofibrils abolishes all force transmission across sarcomeres and all residual
and passive force enhancement. Thus, titin acts as a kind of molecular spring
that increases the muscle’s stiffness, and thus its force, in active compared
with passive muscle contraction. Researchers now speculate that titin
contributes to active force production by changing its stiffness (i.e., when titin
becomes stiffer, it can produce more force). The researchers theorize that
titin’s stiffness increases (1) by binding to calcium upon activation and (2) by
binding to actin and decreasing its length.
Although preliminary results and theoretical models provide support for this
new three-filament model of force production, the molecular details have not
been worked out. If correct, it would provide a substantial update to the classic
cross-bridge theory. If proven, the new three-filament model of muscle
contraction would simultaneously add to our understanding of eccentric
contractions and explain the history-dependent properties of muscle,
information not previously explainable using the classical two-filament crossbridge theory.
Motor Units
Recall that a motor unit is composed of a single α-motor neuron and
the muscle fibers it innervates. The α-motor neuron appears to
determine whether the fibers are type I or type II. The α-motor neuron
in a type I motor unit has a smaller cell body and typically innervates
a cluster of ≤300 muscle fibers. In contrast, the α-motor neuron in a
type II motor unit has a larger cell body and innervates ≥300 muscle
fibers. This difference in the size of motor units means that when a
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single type I α-motor neuron stimulates its fibers, far fewer muscle
fibers contract than when a single type II α-motor neuron stimulates
its fibers. Consequently, type II muscle fibers reach peak tension
faster and collectively generate more force than type I fibers. The
difference in maximal isometric force development between type II
and type I motor units is attributable to two characteristics: the
number of muscle fibers per individual motor unit and the difference in
the size of type II and type I fibers. Type I and type II fibers of the
same diameter generate about the same force. On average, however,
type II fibers tend to be larger than type I fibers, and type II motor
units tend to have more muscle fibers than do the type I motor units.
Distribution of Fiber Types
As mentioned earlier, the percentages of type I and type II fibers are
not the same in all the muscles of the body. Generally, arm and leg
muscles have similar fiber compositions within an individual. An
endurance athlete with a predominance of type I fibers in his or her
leg muscles will likely have a high percentage of type I fibers in the
arm muscles as well. A similar relationship exists for type II fibers.
There are some exceptions, however. The soleus muscle (beneath
the gastrocnemius in the calf), for example, is composed of a very
high percentage of type I fibers in everyone.
Fiber Type and Exercise
Because of these differences in type I and type II fibers, one might
expect that these fiber types would also have different functions when
people are physically active. Indeed, this is the case.
Type I Fibers
In general, type I muscle fibers have a high level of aerobic
endurance. Aerobic means “in the presence of oxygen,” so oxidation
is an aerobic process. Type I fibers are very efficient at producing
ATP from the oxidation of carbohydrate and fat, which is discussed in
chapter 2.
Recall that ATP is required to provide the energy needed for
muscle fiber contraction and relaxation. As long as oxidation occurs,
type I fibers continue producing ATP, allowing the fibers to remain
active. The ability to maintain muscular activity for a prolonged period
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is known as muscular endurance, so type I fibers have high aerobic
endurance. Because of this, they are recruited most often during lowintensity endurance events (e.g., marathon running) and during most
daily activities for which the muscle force requirements are low (e.g.,
walking).
Type II Fibers
Type II muscle fibers, on the other hand, have relatively poor aerobic
endurance when compared to type I fibers. They are better suited to
perform anaerobically (without oxygen). This means that in the
absence of adequate oxygen, ATP is formed through anaerobic
pathways, not oxidative pathways. (We discuss these pathways in
detail in chapter 2.)
Type IIa motor units generate considerably more force than do
type I motor units, but type IIa motor units also fatigue more easily
because of their limited endurance. Thus, type IIa fibers appear to be
the primary fiber type used during shorter, higher-intensity endurance
events, such as the mile run or the 400 m swim.
Although the significance of type IIx fibers is not fully understood,
they apparently are not easily activated by the nervous system. Thus,
they are used rather infrequently in normal, low-intensity activity but
are predominantly used in highly explosive events such as the 100 m
dash and the 50 m sprint swim. Characteristics of the various fiber
types are summarized in table 1.2.
One of the most advanced methods for the study of human muscle
fibers is to dissect fibers out of a muscle biopsy sample, suspend a
single fiber between force transducers, and measure its strength and
single-fiber contractile velocity (Vo). From figure 1.13, one can see
that all of the single fibers tend to reach their peak power when the
fibers are generating only about 20% of their peak force. However, it
is quite clear that the peak power of the type II fibers is considerably
higher than that of the type I fibers.
TABLE 1.2 Structural and Functional Characteristics of
Muscle Fiber Types
Fiber type
Characteristic
Type I
Fibers per motor neuron
≤300
126
Type IIa
Type IIx
Motor neuron size
Motor neuron conduction velocity
Contraction speed (ms)
Type of myosin ATPase
Sarcoplasmic reticulum development
Smaller
Slower
110
Slow
Low
≥300
Larger
Faster
50
Fast
High
≥300
Larger
Faster
50
Fast
High
Determination of Fiber Type
The characteristics of muscle fibers appear to be determined early in
life, perhaps within the first few years. Studies with identical twins
have shown that muscle fiber type, for the most part, is genetically
determined, changing little from childhood to middle age. These
studies reveal that identical twins have nearly identical proportions of
fiber types, whereas fraternal twins differ in their fiber type profiles.
The genes we inherit from our parents likely determine which α-motor
neurons innervate our individual muscle fibers. After innervation is
established, muscle fibers differentiate (become specialized)
according to the type of α-motor neuron that stimulates them. Some
recent evidence, however, suggests that endurance training, strength
training, and muscular inactivity may cause a shift in the myosin
isoforms. Consequently, training may induce a small change, perhaps
less than 10%, in the percentage of type I and type II fibers. Further,
both endurance and resistance training have been shown to reduce
the percentage of type IIx fibers while increasing the fraction of type
IIa fibers.
FIGURE 1.13 (a) The dissection and (b) suspension of a single muscle fiber to study the physiology of
different fiber types. (c) Differences in peak power generated by each fiber type at various percentages
of maximal force.
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Studies of older men and women have shown that aging may alter
the distribution of type I and type II fibers. As we grow older, muscles
tend to lose type II motor units, which increases the percentage of
type I fibers.
In Review
Most skeletal muscles contain both type I and type II fibers.
Different fiber types have different myosin ATPase activities. The ATPase in the
type II fibers acts faster than the ATPase in type I fibers.
Type II fibers have a more highly developed SR, enhancing the delivery of calcium
needed for muscle contraction.
α-Motor
neurons innervating type II motor units are larger and innervate more
fibers than do α-motor neurons for type I motor units. Thus, type II motor units
have more (and larger) fibers to contract and can produce more force than type I
motor units.
The proportions of type I and type II fibers in a person’s arm and leg muscles are
usually similar.
Type I fibers have higher aerobic endurance and are well suited to low-intensity
endurance activities.
Type II fibers are better suited for anaerobic activity. Type IIa fibers play a major
role in high-intensity exercise. Type IIx fibers are activated when the force
demanded of the muscle is high.
Skeletal Muscle and Exercise
Having reviewed the overall structure of muscle, the process by
which it develops force, and the types of muscle fibers, we now look
more specifically at how muscle functions during exercise. Strength,
endurance, and speed depend largely on the muscle’s ability to
produce energy and force. This section examines how muscle
accomplishes this task.
Muscle Fiber Recruitment
When an α-motor neuron carries an action potential to the muscle
fibers in the motor unit, all fibers in the unit develop force. Activating
more motor units is the way muscles produce more force. When little
force is needed, only a few motor units are recruited. Recall from our
earlier discussion that type IIa and type IIx motor units contain more
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muscle fibers than type I motor units do. Skeletal muscle contraction
involves a progressive recruitment of type I, followed by type II motor
units, depending on the requirements of the activity being performed.
As the intensity of the activity increases, the number of fibers
recruited increases in the following order, in an additive manner: type
I → type IIa → type IIx.
Motor units are generally activated on the basis of a fixed order of
fiber recruitment. This is known as the principle of orderly
recruitment, in which the motor units within a given muscle appear to
be ranked. Let’s use the biceps brachii as an example: Assume a
total of 200 motor units, which are ranked on a scale from 1 to 200.
For an extremely fine muscle contraction requiring very little force
production, the motor unit ranked number 1 would be recruited. As
the requirements for force production increase, numbers 2, 3, 4, and
so on would be recruited, up to a maximal muscle contraction that
would activate most, if not all, of the motor units. For the production of
a given force, the same motor units are usually recruited each time
and in the same order.
A mechanism that may partially explain the principle of orderly
recruitment is the size principle, which states that the order of
recruitment of motor units is directly related to the size of their motor
neuron. Motor units with smaller motor neurons will be recruited first.
Because the type I motor units have smaller motor neurons, they are
the first units recruited in graded movement (going from very low to
very high rates of force production). The type II motor units then are
recruited as the force needed to perform the movement increases. It
is unclear at this time how the size principle relates to complex
athletic movements.
During events that last several hours, exercise is performed at a
submaximal pace, and the tension in the muscles is relatively low. As
a result, the nervous system tends to recruit those muscle fibers best
adapted to endurance activity: the type I and some type IIa fibers. As
the exercise continues, these fibers become depleted of their primary
fuel supply (glycogen), and the nervous system must recruit more
type IIa fibers to maintain muscle tension. Finally, when the type I and
type IIa fibers become exhausted, the type IIx fibers may be recruited
to continue exercising.
129
In Review
Motor units give all-or-none responses. Activating more motor units produces
more force.
In low-intensity activity, most muscle force is generated by type I fibers. As the
intensity increases, type IIa fibers are recruited, and at even higher intensities, the
type IIx fibers are activated. The same pattern of recruitment is followed during
events of long duration.
This may explain why fatigue seems to come in stages during
events such as the marathon, a 42 km (26.1 mi) run. It also may
explain why it takes great conscious effort to maintain a given pace
near the finish of the event. This conscious effort results in the
activation of muscle fibers that are not easily recruited. Such
information is of practical importance to our understanding of the
specific requirements of training and performance.
Fiber Type and Athletic Success
From what we have just discussed, it appears that athletes who have
a high percentage of type I fibers might have an advantage in
prolonged endurance events, whereas those with a predominance of
type II fibers could be better suited for high-intensity, short-term, and
explosive activities. But does the relative proportion of an athlete’s
muscle fiber types determine athletic success?
The muscle fiber makeup of successful athletes from a variety of
athletic events and of nonathletes is shown in table 1.3. As
anticipated, the leg muscles of distance runners, who rely on
endurance, have a predominance of type I fibers.4 Studies of elite
male and female distance runners revealed that many of these
athletes’ gastrocnemius (calf) muscles may contain more than 90%
type I fibers. World champions in the marathon are reported to
possess 93% to 99% type I fibers in their gastrocnemius muscles. In
contrast, the gastrocnemius muscles are composed principally of type
II fibers in sprint runners, who rely on speed and strength. Worldclass sprinters have only about 25% type I fibers in this muscle. Also,
although muscle fiber cross-sectional area varies markedly among
elite distance runners, type I fibers in their leg muscles average about
22% more cross-sectional area than type II fibers.5,6 Swimmers tend
130
to have higher percentages of type I fibers (60%-65%) in their arm
muscles than untrained subjects (45%-55%).
The fiber composition of muscles in distance runners and sprinters
is markedly different. However, it may be a bit risky to think we can
select champion distance runners and sprinters solely on the basis of
predominant muscle fiber type. Other factors, such as cardiovascular
function, motivation, training, and muscle size, also contribute to
success in such events of endurance, speed, and strength. Thus,
fiber composition alone is not a reliable predictor of athletic success.
Muscle Contraction
We have examined the different muscle fiber types. We understand
that all fibers in a motor unit, when stimulated, act at the same time
and that different fiber types are recruited in stages, depending on the
force required to perform an activity. Now we can turn our attention to
how whole muscles work to produce movement.
Types of Muscle Contraction
Muscle movement generally can be categorized into three types of
contractions—concentric, static, and eccentric. In many activities,
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such as running and jumping, all three types of contraction may occur
in the execution of a smooth, coordinated movement. For the sake of
clarity, though, we will examine each type separately.
A muscle’s principal action, shortening, is referred to as a
concentric contraction, the most familiar type of contraction. To
understand muscle shortening, recall our earlier discussion of how
the thin and thick filaments slide across each other. In a concentric
contraction, the thin filaments are pulled toward the center of the
sarcomere. Because joint movement is produced, concentric
contractions are considered dynamic contractions.
Muscles can also act without moving. When this happens, the
muscle generates force, but its length remains static (unchanged).
This is called a static (isometric) muscle contraction because the
joint angle does not change. A static contraction occurs, for example,
when one tries to lift an object that is heavier than the force
generated by the muscle, or when one supports the weight of an
object by holding it steady with the elbow flexed. In both cases, the
person feels the muscles tense, but there is no joint movement. In a
static contraction, the myosin cross-bridges form and are recycled,
producing force, but the external force is too great for the thin
filaments to be moved. They remain in their normal position, so
shortening can’t occur. If enough motor units can be recruited to
produce sufficient force to overcome the resistance, a static
contraction can become a dynamic one.
Muscles can exert force even while lengthening. This movement is
an eccentric contraction. Because joint movement occurs, this is
also a dynamic contraction. An example of an eccentric contraction is
the action of the biceps brachii when one extends the elbow slowly to
lower a heavy weight. In this case, the thin filaments are pulled
farther away from the center of the sarcomere, essentially stretching
it.
Generation of Force
Whenever muscles contract, whether the contraction is concentric,
static, or eccentric, the force developed must be graded to meet the
needs of the task or activity. Using golf as an example, the force
needed to tap in a 1 m (~39 in.) putt is far less than that needed to
drive the ball 250 m (273 yd) from the tee to the middle of the fairway.
132
The amount of muscle force developed is dependent on the number
and type of motor units activated, the frequency of stimulation of each
motor unit, the size of the muscle, the muscle fiber and sarcomere
length, and the muscle’s speed of contraction.
More force can be generated when more
motor units are activated. Type II motor units generate more force
than type I motor units because a type II motor unit contains more
muscle fibers than a type I motor unit. In a similar manner, larger
muscles, having more muscle fibers, can produce more force than
smaller muscles.
Motor Units and Muscle Size
A single motor unit
can exert varying levels of force dependent on the frequency at which
it is stimulated. This is illustrated in figure 1.14.1 The smallest
contractile response of a muscle fiber or a motor unit to a single
electrical stimulus is termed a twitch. A series of three stimuli in rapid
sequence, before complete relaxation from the first stimulus, can
elicit an even greater increase in force or tension. This is termed
summation. Continued stimulation at higher frequencies can lead to
the state of tetanus, resulting in the peak force or tension of the
muscle fiber or motor unit. Rate coding is the term used to refer to
the process by which the tension of a given motor unit can vary from
that of a twitch to that of tetanus by increasing the frequency of
stimulation of that motor unit.
Frequency of Stimulation of the Motor Units: Rate Coding
FIGURE 1.14 Variation in force or tension produced based on electrical stimulation frequency,
illustrating the concepts of a twitch, summation, and tetanus.
133
FIGURE 1.15 Variation in force or tension produced (% of maximum) with changes in sarcomere
length, illustrating the concept of optimal length for force production.
Adapted by permission from B.R. MacIntosh, P.F. Gardiner, and A.J. McComas, Skeletal Muscle: Form and
Function, 2nd ed. (Champaign, IL: Human Kinetics, 2006), 156.
Each muscle fiber has an optimal length for
generating force. Recall that each muscle fiber is composed of
sarcomeres connected end to end and that these sarcomeres are
made up of both thick and thin filaments. The optimal sarcomere
length is defined as that length where there is optimal overlap
between the thick and thin filaments. This maximizes the potential for
cross-bridge interaction, as illustrated in figure 1.15.12 When a
sarcomere is overly stretched (1) or shortened (5), little or no force
can be developed since there is little cross-bridge interaction. The
muscle’s resting length is determined by the tendons that attach
muscles to the bones on either end. As it turns out, this natural
resting length maximizes the muscle’s ability to generate force,
referred to as the length–tension relation.
The implication of this relation is that muscle length, and therefore
joint angle, will provide a mechanical advantage for force generation
of a particular muscle or muscle group. The length–tension curve
Length–Tension Relation
134
shown in figure 1.15 illustrates this phenomenon. Maximal tension
can be achieved at sarcomere lengths between 2.0 and 2.25 μm,
where the overlap between myosin and actin is optimal (i.e., the
highest number of cross-bridges can be formed). As the sarcomere
becomes elongated (>2.25 μm), the number of possible cross-bridges
decreases, and therefore tension development (the descending limb
of the curve) decreases accordingly. When sarcomeres are shortened
to lengths <2.0 μm, the ability of myosin to interact with actin
decreases because there are fewer myosin heads available to
interact with actin (actin moves close to the M-line where there are
few myosin heads; see figure 1.5). Another possible explanation for
the reduced ability to produce force at lengths <2.0 μm is the physical
constraint imposed by myosin reaching the Z-line of the sarcomere.
The ability of the muscle to develop force also
depends on the speed of contraction. When people try to lift a very
heavy object, they tend to do it slowly, maximizing the force they can
apply to it. If they grab it and quickly try to lift it, they will likely fail, if
not injure themselves. The force–velocity relation of a muscle
illustrates muscle force as a function of the speed of contraction.
During concentric (muscle-shortening) contractions, maximal force
development decreases progressively as the speed of contraction
increases.
However,
with
eccentric
(muscle-lengthening)
contractions, the opposite is true.
This relation between force development and speed of contraction
can be explained by the number of total cross-bridges attached at
various speeds of contraction. When a muscle is contracting slowly,
there is more time for cross-bridge formation than when contractions
occur at higher speeds. In other words, when cross-bridges are
formed at higher velocities, the ability of the muscle to produce force
is reduced.
The force–velocity relation applies to both shortening and
lengthening contractions. As depicted in figure 1.16, increasing the
velocity of contraction while shortening (moving rightward along the xaxis) reduces force. Another way to think of the force–velocity relation
is in terms of applying an external force to the muscle, such as
performing a biceps curl. As the load gets heavier, the speed of
contraction gets slower. When the load applied equals the maximal
Force–Velocity Relation
135
isometric force of the muscle, contraction velocity equals zero (by
definition, an isometric contraction involves no movement). Now, let’s
explore what will happen when the load applied to the muscle is
higher than the maximal isometric force and the muscle lengthens. In
this case, the ability of the muscle to produce force will increase as a
function of speed (moving leftward along the x-axis in figure 1.16)
because as the load increases beyond maximal isometric, the speed
of contraction will also increase.
FIGURE 1.16 The relation between muscle lengthening and shortening velocity and force production.
Note that the capacity for the muscle to generate force is greater during eccentric (muscle-lengthening)
actions than during concentric (muscle-shortening) actions.
Muscle Memory
136
Muscle force production depends on muscle mass. Because muscle
fibers are large, they need evenly distributed multiple nuclei along
their length in order to support all of the protein synthesis that occurs
within the vast intracellular volume. Muscle fibers constantly change
size, getting smaller with disuse (atrophy) and larger with training
(hypertrophy). Standard thinking has been that muscle precursor
satellite cells, small mononuclear stem cells, multiply during
hypertrophy, fuse with existing muscle fibers, and supply additional
nuclei as the fibers grow in size. Alternatively, during atrophy,
unnecessary nuclei are cleared by a process called apoptosis, or
programmed death.
A newer model has emerged that better explains the mechanisms
that underlie changes in muscle fiber size and muscle mass.3 In a
study by Bruusgaard and colleagues, rat hindlimb muscles were
hypertrophied by overloading, and their nuclei were measured by
injecting labeled nucleotides. Beginning on day 6, the number of
nuclei began to increase, increasing by 54% over 21 days. Fiber
cross-sectional area did not begin to increase until day 9. In another
group of rats, motor nerves were severed, causing muscle atrophy.
The cross-sectional area decreased by 60% of the highest value of
the hypertrophied group, but the number of nuclei was unchanged.
In trained individuals, retraining after a period of disuse occurs
more quickly than in novice exercisers, and such muscle memory has
typically been attributed to neural control of the muscle. It now
appears that the nuclei may be the site of such memory. However, as
pointed out by Lee and Burd,11 a role for satellite cells in muscle
hypertrophy cannot be excluded, and satellite cells undoubtedly
contribute to overall skeletal muscle mass. It is possible that satellite
cells may be necessary to sustain the mass and may be integral in
maintaining muscle quality and function (figure 1.17).
In Review
Among elite athletes, muscle fiber type composition differs by sport and event,
with speed and strength events characterized by higher percentages of type II
fibers and endurance events by higher percentages of type I fibers.
The three main types of muscle contraction are concentric, in which the muscle
shortens; static or isometric, in which the muscle acts but the joint angle is
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unchanged; and eccentric, in which the muscle lengthens.
Force production can be increased both through the recruitment of more motor
units and through an increase in the frequency of stimulation (rate coding) of the
motor units.
Force production is maximized at the muscle’s optimal length. At this length, the
amount of energy stored and the number of linked actin–myosin cross-bridges are
optimal.
Speed of contraction also affects the amount of force produced. For concentric
contraction, maximal force is achieved with slower contractions. The closer to
zero the velocity (isometric), the more force can be generated. With eccentric
contractions, however, faster movement allows more force production.
In addition to satellite cells, preserving the number of muscle fiber nuclei may help
explain why previously trained muscles adapt more quickly to retraining after a
period of disuse.
FIGURE 1.17 (a) A model to explain how the nuclei of muscle fibers may be the site of muscle
memory. This theory explains why previously trained muscles adapt more quickly to retraining after a
period of disuse. (b) Photomicrograph showing peripheral distribution of nuclei within a muscle fiber.
(a) Reprinted from J.C. Bruusgaard et al., “Myonuclei Acquired by Overload Exercise Precede Hypertrophy and are
Not Lost on Detraining,” Proceedings of the National Academy of Sciences 107 (2010): 15111-15116. By permission
of J.C. Bruusgaard
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IN CLOSING
In this chapter, we reviewed the components of skeletal muscle. We considered
the differences in fiber types and their impact on physical performance. We
learned how muscles generate force and produce movement. Now that we
understand how movement is produced, we turn our attention to how movement
is fueled. In the next chapter, we focus on metabolism and energy production.
KEY TERMS
actin
action potential
adenosine triphosphatase (ATPase)
adenosine triphosphate (ATP)
α-motor neuron
concentric contraction
dynamic contraction
eccentric contraction
endomysium
epimysium
excitation–contraction coupling
fascicle
force–velocity relation
length–tension relation
motor unit
muscle fiber
musculoskeletal system
myofibril
myosin
myosin cross-bridge
nebulin
perimysium
plasmalemma
power stroke
principle of orderly recruitment
rate coding
sarcolemma
sarcomere
sarcoplasm
sarcoplasmic reticulum (SR)
139
satellite cells
single-fiber contractile velocity (Vo)
size principle
sliding filament theory
static (isometric) muscle contraction
summation
tetanus
titin
transverse tubules (T-tubules)
tropomyosin
troponin
twitch
type I fiber
type II fiber
STUDY QUESTIONS
1.
2.
3.
4.
5.
6.
List and describe the anatomical components that make up a muscle fiber.
7.
What is the role of genetics in determining the proportions of muscle fiber
types and the potential for success in selected activities?
8.
Describe the relation between muscle force development and the
recruitment of type I and type II motor units.
9.
Explain, and give examples of, how concentric, static, and eccentric
contractions differ.
10.
What two mechanisms are used by the body to increase force production in
a single muscle?
11.
12.
What is the optimal length of a muscle for maximal force development?
13.
14.
In muscle contraction, what roles are played by the protein titin?
List the components of a motor unit.
What are the steps in excitation–contraction coupling?
What is the role of calcium in muscle contraction?
Describe the sliding filament theory. How do muscle fibers shorten?
What are the basic characteristics that differ between type I and type II
muscle fibers?
What is the relation between maximal force development and the speed of
shortening (concentric) and lengthening (eccentric) contractions?
Why do previously trained muscles adapt more quickly to retraining after a
period of disuse?
140
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
141
142
2
Fuel for Exercise: Bioenergetics and
Muscle Metabolism
In this chapter and in the web study guide
Energy Substrates
Carbohydrate
Fat
Protein
AUDIO FOR FIGURE 2.1 describes the path of the three energy substrates in the body.
Controlling the Rate of Energy Production
AUDIO FOR FIGURE 2.2 explains the role of enzymes.
ANIMATION FOR FIGURE 2.3 breaks down a typical metabolic pathway.
VIDEO 2.1 presents Mark Hargreaves discussing the sensitivity of ATP production to muscle activity and
control of ATP production during exercise.
Storing Energy: High-Energy Phosphates
AUDIO FOR FIGURE 2.4 describes the structure and breakdown of ATP.
The Basic Energy Systems
ATP-PCr System
Glycolytic System
Oxidative System
Lactic Acid as a Source of Energy During Exercise
Summary of Substrate Metabolism
ANIMATION FOR FIGURE 2.5 shows the reactions in the ATP-PCr system.
ACTIVITY 2.1 ATP-PCr System reviews the stages in the ATP-PCr system.
AUDIO FOR FIGURE 2.6 describes the changing levels of ATP and PCr during maximal sprinting.
AUDIO FOR FIGURE 2.7 describes the process of glycolysis.
ACTIVITY 2.2 Glycolytic System considers the main steps in the glycolytic system.
AUDIO FOR FIGURE 2.8 describes the overview of the oxidation of carbohydrate.
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AUDIO FOR FIGURE 2.9 describes the Krebs cycle.
ANIMATION FOR FIGURE 2.10 shows the link between the Krebs cycle and the electron transport
chain.
AUDIO FOR FIGURE 2.11 describes the electron transport chain.
ANIMATION FOR FIGURE 2.12 breaks down the total energy production from the oxidation of a
molecule of glucose.
ACTIVITY 2.3 Glucose Oxidation describes how the complete oxidation of glucose produces ATP, heat,
water, and carbon dioxide.
AUDIO FOR FIGURE 2.13 describes the common metabolic pathways for carbohydrate, fat, and
protein.
Interaction of the Energy Systems
AUDIO FOR FIGURE 2.14 describes the relative energy production rate and capacity of the energy
systems.
ACTIVITY 2.4 ATP Production explores three methods of ATP production, depending on the type,
length, and intensity of an activity and the availability of oxygen.
The Crossover Concept
AUDIO FOR FIGURE 2.15 explains the crossover concept.
The Oxidative Capacity of Muscle
Enzyme Activity
Fiber Type Composition and Endurance Training
Oxygen Needs
AUDIO FOR FIGURE 2.16 describes a relationship between enzyme activity and oxidative capacity.
In Closing
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“H
itting the wall” is a common expression heard among marathon
runners, and more than half of all nonelite marathon runners report having hit the
wall during a marathon regardless of how hard they trained. This phenomenon
usually happens around mile 20 to 22. The runner’s pace slows considerably and
the legs feel like lead. Tingling and numbness are often felt in the legs and arms,
and thinking often becomes fuzzy and confused. Hitting the wall is basically running
out of available energy.
The runner’s primary fuel sources during prolonged exercise are carbohydrates
and fats. Fats might seem to be the logical first choice of fuel for endurance events
—they are ideally designed to be energy dense, and stores are virtually unlimited.
Unfortunately, fat metabolism requires a constant supply of oxygen, and delivery of
energy is slower than that provided by carbohydrate metabolism.
Most runners are able to store 2,000 to 2,200 calories of glycogen in their liver
and muscles, which is enough to provide energy for about 20 mi (32 km) of
moderate-pace running. Since the body is much less efficient at converting fat to
energy, running pace slows and the runner suffers from fatigue. Furthermore,
carbohydrates are the sole fuel source for brain function. Physiology, not
coincidence, dictates why so many marathon runners hit the wall at around the 20
mi mark.
Chemical reactions in plants (photosynthesis) convert light from the
sun into stored chemical energy. In turn, humans obtain energy by
eating either plants or animals that feed on plants. Nutrients from
ingested foods are provided in the form of carbohydrates, fats, and
proteins. These three basic fuels, or energy substrates, can
ultimately be broken down to release the stored energy. Each cell
contains chemical pathways that convert these substrates to energy
that can then be used by that cell and other cells of the body, a
process called bioenergetics. All of the chemical reactions in the
body are collectively called metabolism.
Because all energy eventually degrades to heat, the amount of
energy released in a biological reaction can be measured from the
amount of heat produced. Energy in biological systems is measured
in calories. By definition, 1 calorie (cal) equals the amount of heat
energy needed to raise 1 g of water 1 °C, from 14.5 °C to 15.5 °C. In
humans, energy is expressed in kilocalories (kcal), where 1 kcal is
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the equivalent of 1,000 cal. Sometimes the term Calorie (with a
capital C) is used synonymously with kilocalorie, but kilocalorie is
more technically and scientifically correct. Thus, when one reads that
someone eats or expends 3,000 Cal per day, it really means the
person is ingesting or expending 3,000 kcal per day.
Some free energy in the cells is used for growth and repair
throughout the body. Such processes build muscle mass during
training and repair muscle damage after exercise or injury. Energy
also is needed for active transport of many substances, such as
sodium, potassium, and calcium ions, across cell membranes to
maintain homeostasis. Myofibrils use energy to cause sliding of the
actin and myosin filaments, resulting in muscle action and force
generation, as described in chapter 1.
Energy Substrates
Energy is released when chemical bonds—the bonds that hold
elements together to form molecules—are broken. Substrates are
composed primarily of carbon, hydrogen, oxygen, and (in the case of
protein) nitrogen. The molecular bonds that hold these elements
together are relatively weak and therefore provide little energy when
broken. Consequently, food is not used directly for cellular operations.
Rather, the energy in food’s molecular bonds is chemically released
within our cells and then stored in the form of the high-energy
compound introduced in chapter 1, adenosine triphosphate (ATP),
which is discussed in detail later in this chapter.
At rest, the energy that the body needs is derived almost equally
from the breakdown of carbohydrates and fats. Proteins serve
important functions as enzymes that aid chemical reactions and as
structural building blocks but usually provide little energy for
metabolism. During intense, short-duration muscular effort, more
carbohydrate is used, with less reliance on fat to generate ATP.
Longer, less intense exercise uses both carbohydrate and fat for
sustained energy production.
Carbohydrate
The amount of carbohydrate used during exercise is related to both
the carbohydrate availability and the muscles’ well-developed system
for carbohydrate metabolism. All carbohydrates are ultimately
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converted to the simple six-carbon sugar, glucose (figure 2.1), a
monosaccharide (one-unit sugar) that is transported through the
blood to all body tissues. Under resting conditions, ingested
carbohydrate is stored in muscles and liver in the form of a more
complex polysaccharide (multiple linked sugar molecules), glycogen.
Glycogen is stored in the cytoplasm of muscle cells until those cells
use it to form ATP. Additional glycogen stored in the liver is converted
back to glucose as needed and then transported by the blood to
active tissues, where it is metabolized.
Muscle and liver glycogen stores are limited, especially if the diet
contains an insufficient amount of carbohydrate, and can be depleted
during prolonged, intense exercise. Thus, we rely heavily on dietary
sources of starches and sugars to continually replenish our
carbohydrate reserves. Without adequate carbohydrate intake,
muscles can be deprived of their primary energy source.
Furthermore, carbohydrates are the only energy source used by brain
tissue; therefore, severe carbohydrate depletion results in negative
cognitive effects.
FIGURE 2.1 Cellular metabolism results from the breakdown of three fuel substrates provided by the
diet. Once each is converted to its usable form, it either circulates in the blood as an available “pool” to
be used for metabolism or is stored in the body.
147
Fat
Fats provide a large portion of the energy used during prolonged, less
intense exercise. Body stores of potential energy in the form of fat are
substantially larger than the reserves of carbohydrate, in terms of
both weight and energy availability. Table 2.1 provides an indication of
the total body stores of these two energy sources in a lean person
(12% body fat). For the average middle-aged adult with more body fat
(adipose tissue), the fat stores would be approximately twice as large,
whereas the carbohydrate stores would be about the same. But fat is
less readily available for cellular metabolism because it must first be
reduced from its complex form, triglyceride, to its basic components,
glycerol and free fatty acids (FFAs). Only FFAs are used to form
ATP (figure 2.1).
TABLE 2.1 Body Stores of Fuels and Associated Energy
Availability
Location
g
kcal
110
500
15
451
2,050
62
7,800
161
7,961
73,320
1,513
74,833
Carbohydrate
Liver glycogen
Muscle glycogen
Glucose in body fluids
Fat
Subcutaneous and visceral
Intramuscular
Total
Note. These estimates are based on a body weight of 65 kg (143 lb) with 12% body fat.
Substantially more energy is derived from breaking down a gram of
fat (9.4 kcal/g) than from the same amount of carbohydrate (4.1
kcal/g). Nonetheless, the rate of energy release from fat is too slow to
meet all of the energy demands of intense muscular activity.
Other types of fats found in the body serve non-energy-producing
functions. Phospholipids are a key structural component of all cell
membranes and form protective sheaths around some large nerves.
Steroids are found in cell membranes and also function as hormones
or as building blocks of hormones, such as estrogen and
testosterone.
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Protein
Protein can be used as a minor energy source under some
circumstances, but it must first be converted into glucose (figure 2.1).
In the case of severe energy depletion or starvation, protein may
even be used to generate FFAs for energy. The process by which
protein or fat is converted into glucose is called gluconeogenesis.
The process of converting protein into fatty acids is termed
lipogenesis. Protein can supply up to 10% of the energy needed to
sustain prolonged exercise. Only the most basic units of protein—the
amino acids—can be used for energy. A gram of protein yields about
4.1 kcal.
Controlling the Rate of Energy Production
To be useful, free energy must be released from chemical
compounds at a controlled rate. This rate is determined primarily by
two things, the availability of the primary substrate and enzyme
activity. The availability of large amounts of a substrate increases the
activity of that particular pathway. An abundance of one particular fuel
(e.g., carbohydrate) can cause cells to rely more on that source than
on alternatives. This influence of substrate availability on the rate of
metabolism is termed the mass action effect.
Specific protein molecules called enzymes also control the rate of
free-energy release. Many of these enzymes speed up the
breakdown (catabolism) of chemical compounds. Chemical
reactions occur only when the reacting molecules have sufficient
initial energy to start the reaction or chain of reactions. Enzymes do
not cause a chemical reaction to occur and do not determine the
amount of usable energy that is produced by these reactions. Rather,
they speed up reactions by lowering the activation energy that is
required to begin the reaction (figure 2.2).
Although the enzyme names are quite complex, most end with the
suffix -ase. For example, an important enzyme that breaks down ATP
and releases stored energy is adenosine triphosphatase, better
known as ATPase.
Biochemical pathways that result in the production of a product
from a substrate almost always involve multiple steps. Each individual
step is typically catalyzed by a specific enzyme. Therefore, increasing
149
the amount of enzyme present or the activity of that enzyme (for
example, by changing the temperature or pH) results in an increased
rate of product formation through that metabolic pathway. Additionally,
many enzymes require other molecules called cofactors to function,
so cofactor availability may also affect enzyme function and therefore
the rate of metabolic reactions.
As illustrated in figure 2.3, metabolic pathways typically have one
enzyme that is of particular importance in controlling the reaction’s
overall rate. This enzyme, usually located in an early step in the
pathway, is known as the rate-limiting enzyme. The activity of a
rate-limiting enzyme is determined by the accumulation of substances
farther down the pathway that decrease enzyme activity through
negative feedback.
FIGURE 2.2 Enzymes control the rate of chemical reactions by lowering the activation energy required
to initiate the reaction. In this example, the enzyme creatine kinase binds to its substrate
phosphocreatine to increase the rate of production of creatine.
Adapted from original figure provided by Dr. Martin Gibala, McMaster University, Hamilton, Ontario, Canada.
150
FIGURE 2.3 A typical metabolic pathway showing the important role of enzymes in controlling the rate
of the reaction. An input of energy in the form of stored adenosine triphosphate (ATP) is needed to begin
the series of reactions (activation energy), but less initial energy is needed if one or more enzymes are
involved in this activation step. As fuels are subsequently degraded into by-products along the metabolic
pathway, ATP is formed. Utilization of the stored ATP results in the release of usable energy, heat, and
the release of adenosine diphosphate (ADP) and inorganic phosphate (Pi).
In Review
Energy for cell metabolism is derived from three substrates in foods:
carbohydrate, fat, and protein. Proteins provide little of the energy used for
metabolism under normal conditions.
Within cells, the usable storage form of the energy we derive from food is the
high-energy compound adenosine triphosphate, or ATP.
Carbohydrate and protein each provide about 4.1 kcal energy per gram,
compared with about 9.4 kcal/g for fat.
Carbohydrate, stored as glycogen in muscle and the liver, is more quickly
accessible as an energy source than either protein or fat. Glucose, directly from
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food or broken down from stored glycogen, is the usable form of carbohydrate.
Fat, stored as triglycerides in adipose tissue, is an ideal storage form of energy.
Free fatty acids from the breakdown of triglycerides are converted to energy.
Carbohydrate stores in the liver and skeletal muscle are limited to about 2,500 to
2,600 kcal of energy, or the equivalent of the energy needed for about 40 km (25
mi) of running. Fat stores can provide more than 70,000 kcal of energy.
Enzymes control the rate of metabolism and energy production. Enzymes can
speed up the overall reaction by lowering the initial activation energy and by
catalyzing various steps along the pathway.
Enzymes can be inhibited through negative feedback of subsequent pathway byproducts (or often ATP), slowing the overall rate of the reaction. This usually
involves a particular enzyme located early in the pathway called the rate-limiting
enzyme.
One example of a substance that may accumulate and feed back
to decrease enzyme activity would be the end product of the
pathway; another would be ATP and its breakdown products, ADP
and inorganic phosphate. If the goals of a metabolic pathway are to
form a chemical product and release free energy in the form of ATP, it
makes sense that an abundance of either that end product or ATP
would feed back to slow further production and release, respectively.
VIDEO 2.1 Presents Mark Hargreaves discussing the sensitivity
of ATP production to muscle activity and control of ATP production
during exercise.
Storing Energy: High-Energy Phosphates
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The immediately available source of energy for almost all bodily
functions, including muscle contraction, is ATP. An ATP molecule
(figure 2.4a) is composed of adenosine (a molecule of adenine joined
to a molecule of ribose) combined with three inorganic phosphate (Pi)
groups. Adenine is a nitrogen-containing base, and ribose is a fivecarbon sugar. When an ATP molecule is combined with water
(hydrolysis) and acted on by the enzyme ATPase, the last phosphate
group splits away, rapidly releasing a large amount of free energy
(approximately 7.3 kcal per mole of ATP under standard conditions,
but possibly up to 10 kcal per mole of ATP or greater within the cell).
This reduces the ATP to adenosine diphosphate (ADP) and Pi
(figure 2.4b).
To generate ATP, a phosphate group is added to the relatively lowenergy compound, ADP, in a process called phosphorylation. This
process requires a considerable amount of energy. Some ATP is
generated independent of oxygen availability, and such metabolism is
called substrate-level phosphorylation. Other ATP-producing
reactions (discussed later in the chapter) occur without oxygen, while
still others occur with the aid of oxygen, a process called oxidative
phosphorylation.
As shown in figure 2.3, ATP is formed from ADP and Pi via
phosphorylation as fuels are broken down into fuel by-products at
various steps along a metabolic pathway. The storage form of energy,
ATP, can subsequently release free or usable energy when needed
as it is once again broken down into ADP and Pi.
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FIGURE 2.4 (a) The structure of an adenosine triphosphate (ATP) molecule, showing the high-energy
phosphate bonds. (b) When the third phosphate on the ATP molecule is separated from adenosine by
the action of adenosine triphosphatase (ATPase), energy is released.
The Basic Energy Systems
Cells can store only very limited amounts of ATP and must constantly
generate new ATP to provide needed energy for all cellular
metabolism, including muscle contraction. Cells generate ATP
through any one of (or a combination of) three metabolic pathways:
1. The ATP-PCr system
2. The glycolytic system (glycolysis)
3. The oxidative system (oxidative phosphorylation)
The first two systems can act in the absence of oxygen and are jointly
termed anaerobic metabolism. The third system requires oxygen
and therefore comprises aerobic metabolism.
ATP-PCr System
The simplest of the energy systems is the ATP-PCr system, shown
in figure 2.5. In addition to storing a very small amount of adenosine
154
triphosphate (ATP) directly, cells contain another high-energy
phosphate molecule that stores energy called phosphocreatine
(PCr; sometimes called creatine phosphate). This simple pathway
involves donation of a Pi from PCr to ADP to form ATP. Unlike what
occurs with the limited freely available ATP in the cell, energy
released by the breakdown of PCr is not directly used for cellular
work. Instead, it regenerates ATP to maintain a relatively constant
supply under resting conditions.
The release of energy from PCr is catalyzed by the enzyme
creatine kinase, which acts on PCr to separate Pi from creatine. The
energy released can then be used to add a Pi molecule to an ADP
molecule, forming ATP. As energy is released from ATP by the
splitting of a phosphate group, cells can prevent ATP depletion by
breaking down PCr, providing energy and Pi to re-form ATP from
ADP.
Following the principles of negative feedback and rate-limiting
enzymes discussed earlier, creatine kinase activity is enhanced when
concentrations of ADP or Pi increase, and is inhibited when ATP
concentrations increase. When intense exercise is initiated, the small
amount of available ATP in muscle cells is broken down for
immediate energy, yielding ADP and Pi. The increased ADP
concentration enhances creatine kinase activity, and PCr is
catabolized to form additional ATP. As exercise progresses and
additional ATP is generated by the other two energy systems—the
glycolytic and oxidative systems—creatine kinase activity is inhibited.
This process of breaking down PCr to allow formation of ATP is
rapid and can be accomplished without any special structures within
the cell. The ATP-PCr system is classified as substrate-level
metabolism. Although it can act in the presence of oxygen, the
process does not require oxygen.
During the first few seconds of intense muscular activity, such as
sprinting, ATP is maintained at a relatively constant level, but PCr
declines steadily as it is used to replenish the depleted ATP (see
figure 2.6). At exhaustion, however, both ATP and PCr levels are low
and are unable to provide energy for further muscle contraction and
relaxation. Thus, the capacity to maintain ATP levels with the energy
from PCr is limited. The combination of ATP and PCr stores can
155
sustain the muscles’ energy needs for only 3 to 15 s during an all-out
sprint. Beyond that time, muscles must rely on other processes for
ATP formation: glycolytic and oxidative pathways.
FIGURE 2.5 In the ATP-PCr system, adenosine triphosphate (ATP) can be recreated via the binding of
an inorganic phosphate (Pi) to adenosine diphosphate (ADP) with the energy derived from the
breakdown of phosphocreatine (PCr).
156
FIGURE 2.6 Changes in type II (fast-twitch) skeletal muscle adenosine triphosphate (ATP) and
phosphocreatine (PCr) during 14 s of maximal muscular effort (sprinting). Although ATP is being used at
a very high rate, the energy from PCr is used to synthesize ATP, initially preventing the ATP level from
decreasing. However, at exhaustion, both ATP and PCr levels are low.
Glycolytic System
The ATP-PCr system has a limited capacity to generate ATP for
energy, lasting only a few seconds. The second method of ATP
production involves the liberation of energy through the breakdown
(“lysis”) of glucose. This system is called the glycolytic system
because it entails glycolysis, the breakdown of glucose through a
pathway that involves a sequence of glycolytic enzymes. Glycolysis is
a more complex pathway than the ATP-PCr system, and the
sequence of steps involved in this process is presented in figure 2.7.
157
FIGURE 2.7 The derivation of energy (ATP) by glycolysis. Glycolysis involves the breakdown of one
glucose (six-carbon) molecule to two three-carbon molecules of pyruvic acid. The process can begin
with either glucose circulating in the blood or glycogen (a chain of glucose molecules, the storage form
of glucose in muscle and liver). Note that there are roughly 10 separate steps in this anaerobic process,
and the net result is the generation of either two or three ATP molecules, depending on whether glucose
or glycogen is the initial substrate.
Glucose accounts for about 99% of all sugars circulating in the
blood. Blood glucose comes from the digestion of carbohydrate and
the breakdown of liver glycogen. Glycogen is synthesized from
158
glucose by a process called glycogenesis and is stored in the liver or
in muscle until needed. At that time, the glycogen is broken down to
glucose-1-phosphate, which enters the glycolysis pathway, a process
termed glycogenolysis.
Before either glucose or glycogen can be used to generate energy,
it must be converted to a compound called glucose-6-phosphate.
Even though the goal of glycolysis is to release ATP, the conversion
of a molecule of glucose to glucose-6-phosphate requires the
expenditure or input of one ATP molecule. In the conversion of
glycogen, glucose-6-phosphate is formed from glucose-1-phosphate
without this energy expenditure. Glycolysis technically begins once
the glucose-6-phosphate is formed.
Glycolysis requires 10 to 12 enzymatic reactions for the breakdown
of glycogen to pyruvic acid, which is then converted to lactic acid. All
steps in the pathway and all of the enzymes involved operate within
the cell cytoplasm. The net gain from this process is 3 moles (mol) of
ATP formed for each mole of glycogen broken down. If glucose is
used instead of glycogen, the gain is only 2 mol of ATP because 1
mol was used for the conversion of glucose to glucose-6-phosphate.
This energy system obviously does not produce large amounts of
ATP. Despite this limitation, the combined actions of the ATP-PCr and
glycolytic systems allow the muscles to generate force even when the
oxygen supply is limited. These two systems predominate during the
early minutes of high-intensity exercise.
Another major limitation of anaerobic glycolysis is that it causes an
accumulation of lactic acid in the muscles and body fluids. Glycolysis
produces pyruvic acid. This process does not require oxygen, but the
presence of oxygen determines the fate of the pyruvic acid. Without
oxygen present, the pyruvic acid is converted directly to lactic acid,
an acid with the chemical formula C3H6O3 that quickly dissociates,
forming lactate. The terms pyruvic acid and pyruvate, and lactic acid
and lactate, are often used interchangeably in exercise physiology. In
each case, the acid form of the molecule is relatively unstable at
normal body pH and rapidly loses a hydrogen ion. The remaining
molecule is more correctly called pyruvate or lactate. Lactate can
itself be a source of energy as discussed later in this chapter.
159
In all-out sprint events lasting 1 or 2 min, the demands on the
glycolytic system are high, and muscle lactic acid concentrations can
increase from a resting value of about 1 mmol/kg of muscle to more
than 25 mmol/kg. This acidification of muscle fibers inhibits further
glycogen breakdown because it impairs glycolytic enzyme function. In
addition, the acid decreases the fibers’ calcium-binding capacity and
thus may impede muscle contraction.
The rate-limiting enzyme in the glycolytic pathway is
phosphofructokinase (PFK). Like almost all rate-limiting enzymes,
PFK catalyzes an early step in the pathway, the conversion of
fructose-6-phosphate to fructose-1,6-diphosphate. Increasing ADP
and Pi concentrations enhance PFK activity and therefore speed up
glycolysis, while elevated ATP concentrations slow glycolysis by
inhibiting PFK. Additionally, because the glycolytic pathway feeds into
the Krebs cycle for additional energy production when oxygen is
present (discussed later), products of the Krebs cycle, especially
citrate and hydrogen ions, likewise feedback to inhibit PFK.
A muscle fiber’s rate of energy use during exercise can be 200
times greater than at rest. The ATP-PCr and glycolytic systems alone
cannot supply all the needed energy. Furthermore, these two systems
are not capable of supplying all of the energy needs for all-out activity
lasting more than 2 min or so. Prolonged exercise relies on the third
energy system, the oxidative system.
In Review
The formation of ATP provides cells with a high-energy compound for storing and,
when broken down, releasing energy. It serves as the immediate source of energy
for most body functions, including muscle contraction.
Adenosine triphosphate is generated through three primary energy systems:
1.
2.
3.
The ATP-PCr system
The glycolytic system
The oxidative system
In the ATP-PCr system, Pi is separated from PCr through the action of creatine
kinase. The Pi can then combine with ADP to form ATP using the energy released
from the breakdown of PCr. This system is anaerobic, and its main function is to
maintain ATP levels early in exercise. The energy yield is 1 mol of ATP per 1 mol
of PCr.
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The glycolytic system involves the process of glycolysis, through which glucose or
glycogen is broken down to pyruvic acid. When glycolysis occurs without oxygen,
the pyruvic acid is converted to lactic acid. One mole of glucose yields 2 mol ATP,
but 1 mol glycogen yields 3 mol ATP.
The ATP-PCr and glycolytic systems are major contributors of energy during
short-burst activities lasting up to 2 min and during the early minutes of longer
high-intensity exercise.
Oxidative System
The final system of cellular energy production is the oxidative
system. This is the most complex of the three energy systems, and
only a brief overview is provided here. The process by which the body
breaks down substrates with the aid of oxygen to generate energy is
called cellular respiration. Because oxygen is required, this is an
aerobic process. Unlike the anaerobic production of ATP that occurs
in the cytoplasm of the cell, the oxidative production of ATP occurs
within special cell organelles called mitochondria. In muscles, these
are adjacent to the myofibrils and are also scattered throughout the
sarcoplasm (see figure 1.3).
The total number, or density, of mitochondria within a muscle fiber
is determined by its demand for ATP production, but the precise
location of these mitochondria within the cell is determined by oxygen
diffusion. Each individual muscle fiber has an optimal distribution of
mitochondria within the cell that allows for a near maximal rate of ATP
production while exposing the mitochondria to as little excess oxygen
as possible. Excess oxygen exposure in mitochondria creates
reactive oxygen species (ROS), which are toxic to the cell at high
concentrations.5,7
Within a muscle cell, mitochondria tend to be localized along the
periphery of the fiber, with higher densities near capillaries. This
arrangement functions to create gradients in the oxygen
concentration from the capillary to the mitochondria to facilitate the
flow of oxygen into the mitochondria. Having mitochondria localized
toward the periphery of the cell benefits the muscle fiber by
optimizing oxygen delivery to sustain high metabolic rates.6 However,
having the mitochondria located around the periphery of the cell also
increases ROS production because of their exposure to oxygen.
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Thus, mitochondria tend to be distributed nonuniformly around the
outside of the cell, depending on capillary location, rather than being
evenly spaced. This location is optimal for maintaining high metabolic
rates while minimizing risk for increasing ROS production, which can
negatively affect the cell.
Muscles need a steady supply of energy to continuously produce
the force needed during long-term activity. Unlike what happens with
anaerobic ATP production, the oxidative system is slow to turn on, but
it has a much larger energy-producing capacity, so aerobic
metabolism is the primary method of energy production during
endurance activities. This places considerable demands on the
cardiovascular and respiratory systems to deliver oxygen to the active
muscles. Oxidative energy production can come from carbohydrates
(starting with glycolysis) or fats.
Oxidation of Carbohydrate
As shown in figure 2.8, oxidative production of ATP from
carbohydrates involves three processes:
Glycolysis (figure 2.8a)
The Krebs cycle (figure 2.8b)
The electron transport chain (figure 2.8c)
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FIGURE 2.8 In the presence of oxygen, after glucose (or glycogen) has been reduced to pyruvate, (a)
the pyruvate is first catalyzed to acetyl coenzyme A (acetyl CoA), which can enter (b) the Krebs cycle,
where oxidative phosphorylation occurs. Hydrogen ions released during the Krebs cycle then combine
with coenzymes that carry the hydrogen ions to (c) the electron transport chain.
In carbohydrate metabolism, glycolysis plays a role in both
anaerobic and aerobic ATP production. The process of glycolysis is
the same regardless of whether oxygen is present. The presence of
oxygen determines only the fate of the end product, pyruvic acid.
Recall that anaerobic glycolysis produces lactic acid and only three
net moles of ATP per mole of glycogen, or two net moles of ATP per
mole of glucose. In the presence of oxygen, however, the pyruvic acid
is converted into a compound called acetyl coenzyme A (acetyl
CoA).
Glycolysis
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Once formed, acetyl CoA enters the Krebs cycle (also
called the citric acid cycle or tricyclic acid cycle), a complex series of
chemical reactions that permit the complete oxidation of acetyl CoA
(see figure 2.9). Recall that for every glucose molecule that enters the
glycolytic pathway, two molecules of pyruvate are formed. Therefore,
each glucose molecule that begins the energy-producing process in
the presence of oxygen results in two complete Krebs cycles.
As depicted in 2.8b (and shown in more detail in figure 2.9), the
conversion of succinyl CoA to succinate in the Krebs cycle results in
the generation of guanosine triphosphate, or GTP, a high-energy
compound similar to ATP. Guanosine triphosphate then transfers a Pi
to ADP to form ATP. These two ATPs (per molecule of glucose) are
formed by substrate-level phosphorylation. So at the end of the Krebs
cycle, two additional moles of ATP have been formed directly, and the
original carbohydrate has been broken down into carbon dioxide and
hydrogen.
As in the other pathways involved in energy metabolism, Krebs
cycle enzymes are regulated by negative feedback at several steps in
the cycle. The rate-limiting enzyme in the Krebs cycle is isocitrate
dehydrogenase, which, like PFK, is inhibited by ATP and activated by
ADP and Pi as is the electron transport chain. Because muscle
contraction relies on the availability of calcium in the cell, excess
calcium also stimulates the rate-limiting enzyme isocitrate
dehydrogenase.
Krebs Cycle
During glycolysis, hydrogen ions are released
when glucose is metabolized to pyruvic acid. Additional hydrogen
ions are released in the conversion of pyruvate to acetyl CoA and at
several steps in the Krebs cycle. If these hydrogen ions remained in
the system, the inside of the cell would become too acidic. What
happens to this hydrogen?
The Krebs cycle is coupled to a series of reactions known as the
electron transport chain (figure 2.8c). The hydrogen ions released
during the processes of glycolysis, the conversion of pyruvic acid to
acetyl CoA, and the Krebs cycle combine with two coenzymes:
nicotinamide adenine dinucleotide (NAD) and flavin adenine
dinucleotide (FAD), converting each to its reduced form (NADH and
FADH2, respectively). During each Krebs cycle, three molecules of
Electron Transport Chain
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NADH and one molecule of FADH2 are produced. These carry the
hydrogen atoms (electrons) to the electron transport chain, a group of
mitochondrial protein complexes located in the inner mitochondrial
membrane (figure 2.10).
FIGURE 2.9 The series of reactions that take place during the Krebs cycle, showing the compounds
formed and enzymes involved.
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These protein complexes contain a series of enzymes and ironcontaining proteins known as cytochromes. These proteins serve as
electron magnets that transfer electrons, where the first complex,
flavin mononucleotide (FMN), is a stronger magnet for electrons than
NADH, the second complex is a stronger magnet than the first, and
so on down the chain. As high-energy electrons are passed from
complex to complex along this chain, some of the energy released by
those reactions is used to pump H+ from the mitochondrial matrix into
the outer mitochondrial compartment. As these hydrogen ions move
back across the membrane down their concentration gradient, energy
is transferred to ADP, and ATP is formed. This final step requires an
enzyme known as ATP synthase. At the end of the chain, the H+
combines with oxygen to form water, thus preventing acidification of
the cell. This is illustrated in figure 2.11. Because this overall process
relies on oxygen as the final acceptor of electrons and H+, it is
referred to as oxidative phosphorylation.
FIGURE 2.10 Locations of the processes of glycolysis (cytoplasm), the Krebs cycle (mitochondria), and
the electron transport chain (inner mitochondrial membrane).
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FIGURE 2.11 The final step in the aerobic production of adenosine triphosphate (ATP) is the transfer of
energy from the high-energy electrons of reduced nicotinamide adenine dinucleotide (NADH) and
reduced flavin adenine dinucleotide (FADH2) within the mitochondria, following a series of steps known
as the electron transport chain.
For every pair of electrons transported to the electron transport
chain by NADH, three molecules of ATP are formed, while the
electrons passed through the electron transport chain by FADH2 yield
only two molecules of ATP. However, because the NADH and FADH2
are outside the membrane of the mitochondria, the H+ must be
shuttled through the membrane, which requires energy to be used.
So, in reality, the net yields are only 2.5 ATPs per NADH and 1.5
ATPs per FADH2.
The complete oxidation of
glucose can generate 32 molecules of ATP, while 33 ATPs are
produced from one molecule of muscle glycogen. The sites of ATP
production are summarized in figure 2.12. The net production of ATP
Energy Yield From Oxidation of Carbohydrate
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from substrate-level phosphorylation in the glycolytic pathway leading
into the Krebs cycle results in a net gain of two ATPs (or three from
glycogen). A total of 10 NADH molecules leading into the electron
transport chain—two in glycolysis, two in the conversion of pyruvic
acid to acetyl CoA, and six in the Krebs cycle—yields 25 net ATP
molecules. Remember that while 30 ATPs are actually produced, the
energy cost of transporting ATP across membranes uses five of those
ATPs. The two FAD molecules in the Krebs cycle that are involved in
electron transport result in three additional net ATPs. And finally,
substrate-level phosphorylation within the Krebs cycle involving the
molecule GTP adds another two ATP molecules.
Accounting for the energy cost of shuttling electrons across the
mitochondrial membrane is a relatively new concept in exercise
physiology, and many textbooks still refer to net energy productions of
36 to 39 ATPs per molecule of glucose.
Oxidation of Fat
As noted earlier, fat also contributes importantly to the muscle’s
energy needs. Muscle and liver glycogen stores can provide only
~2,500 kcal of energy, but the fat stored inside muscle fibers and in
fat cells can supply at least 70,000 to 75,000 kcal, even in a lean
adult. Although many chemical compounds (such as triglycerides,
phospholipids, and cholesterol) are classified as fats, only
triglycerides are major energy sources. Triglycerides are stored in fat
cells and between and within skeletal muscle fibers. To be used for
energy, a triglyceride must be broken down to its basic units: one
molecule of glycerol and three FFA molecules. This process is called
lipolysis and is controlled by enzymes known as lipases.
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FIGURE 2.12 The net energy production from the oxidation of one molecule of glucose is 32 molecules
of adenosine triphosphate (ATP). Oxidation of glycogen as the original substrate would yield one
additional ATP.
Free fatty acids are the primary energy source for fat metabolism.
Once liberated from glycerol, FFAs can enter the blood and be
transported throughout the body, entering muscle fibers by either
simple diffusion or transporter-mediated (facilitated) diffusion. Their
rate of entry into the muscle fibers depends on the concentration
gradient. Increasing the concentration of FFAs in the blood increases
the rate of their transport into muscle fibers.
Recall that fats are stored in the body in two places,
within muscle fibers and in adipose tissue cells called adipocytes.
The storage form of fats is triglyceride, which is broken down into
FFAs and glycerol for energy metabolism. Before FFAs can be used
for energy production, they must be converted to acetyl CoA in the
mitochondria, a process called β-oxidation. Acetyl CoA is the
β-Oxidation
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common intermediate through which all substrates enter the Krebs
cycle for oxidative metabolism.
β-Oxidation is a series of steps in which two-carbon acyl units are
chopped off of the carbon chain of the FFA. The acyl units become
acetyl CoA, which then enters the Krebs cycle for the formation of
ATP. The number of steps depends on the number of carbons in the
FFA, usually between 14 and 24 carbons. For example, if an FFA
originally has a 16-carbon chain, β-oxidation yields eight molecules of
acetyl CoA.
On entering the muscle fiber, FFAs must be enzymatically
activated with energy from ATP, preparing them for catabolism
(breakdown) within the mitochondria. Like glycolysis, β-oxidation
requires an input energy of two ATPs for activation but, unlike
glycolysis, produces no ATPs directly.
After β-oxidation, fat
metabolism follows the same path as oxidative carbohydrate
metabolism. Acetyl CoA formed by β-oxidation enters the Krebs
cycle. The Krebs cycle generates hydrogen, which is transported to
the electron transport chain along with the hydrogen generated during
β-oxidation to undergo oxidative phosphorylation. As in glucose
metabolism, the by-products of FFA oxidation are ATP, H2O, and
carbon dioxide (CO2). However, the complete combustion of an FFA
molecule requires more oxygen because an FFA molecule contains
considerably more carbon molecules than a glucose molecule.
The advantage of having more carbon molecules in FFAs than in
glucose is that more acetyl CoA is formed from the metabolism of a
given amount of fat, so more acetyl CoA enters the Krebs cycle and
more electrons are sent to the electron transport chain. This is why
fat metabolism can generate much more energy than glucose
metabolism. Unlike glucose or glycogen, fats are heterogeneous, and
the amount of ATP produced depends on the specific fat oxidized.
Krebs Cycle and the Electron Transport Chain
RESEARCH PERSPECTIVE 2.1
White, Brown, and (Perhaps) Beige Fat in Humans
Brown adipose tissue (BAT), often called brown fat, is found in almost every
species of mammal, especially in those that hibernate. Unlike white adipose
tissue, which is specialized for lipid storage and breakdown (lipolysis) to meet
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long-duration metabolic demands, the function of brown adipose is to transfer
energy from food directly into heat. Brown adipose cells contain many small
lipid droplets and many mitochondria, which give the tissue its brown
appearance. BAT cells also have more blood vessels than white adipose cells
to supply the tissue with oxygen and nutrients and distribute the heat
produced in the cells to the rest of the body. The inner membrane of the
mitochondria of BAT cells has a specialized protein called uncoupling protein
that uncouples the electron transport chain from the creation of ATP
(phosphorylation). While white fat generates ATP for energy, brown fat’s
primary role is to produce heat and increase metabolism, especially at rest.
Brown adipose is abundant in newborn babies and young children.
However, for a long time, it was believed that brown adipose stores were
absent in adult humans. In 2009, a study published in the New England
Journal of Medicine showed that adult humans have functionally active brown
adipose tissue.3 Using positron-emission tomography and computed
tomography (PET-CT) scans, researchers found that the most common
location for this brown adipose tissue in adults was near the clavicles, that
brown adipose was more frequently found in women than in men, and that
individuals with a higher body mass index have less brown fat. Because BAT
promotes energy dissipation rather than energy storage (the role of white
adipose tissue), its discovery in humans sparked great interest in the
possibility of increasing the activity of BAT to target diseases like obesity and
type 2 diabetes.
Several studies have recently reported that chronic endurance exercise
may promote the expression of similar thermogenic (heat-producing) genes in
white adipose tissue, resulting in the browning of white fat. In one animal
study, training-induced changes in fat type resulted in increases in resting
energy expenditure of up to 17% in trained rats.2 It is still unclear whether
exercise training increases BAT mass or promotes the browning of white
adipose tissue in humans, but studies are now underway to use the metabolic
potential of BAT to increase whole-body energy expenditure. The ultimate goal
of these studies is to treat obesity and other metabolic diseases.
Consider the example of palmitic acid, a rather abundant 16carbon FFA. The combined reactions of oxidation, the Krebs cycle,
and the electron transport chain produce 106 molecules of ATP from
one molecule of palmitic acid (see table 2.2), compared with only 32
molecules of ATP from glucose or 33 from glycogen.
Oxidation of Protein
As noted earlier, carbohydrates and fatty acids are the preferred fuel
substrates. But proteins, or rather the amino acids that compose
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proteins, are also used for energy under some circumstances. Some
amino acids can be converted into glucose, a process called
gluconeogenesis (see figure 2.1). Alternatively, some can be
converted into various intermediates of oxidative metabolism (such as
pyruvate or acetyl CoA) to enter the oxidative process.
Protein’s energy yield is not as easily determined as that of
carbohydrate or fat because protein also contains nitrogen. When
amino acids are catabolized, some of the released nitrogen is used to
form new amino acids, but the remaining nitrogen cannot be oxidized
by the body. Instead it is converted into urea and then excreted,
primarily in the urine. This conversion requires the use of ATP, so
some energy is spent in this process.
When protein is broken down through combustion in the laboratory,
the energy yield is 5.65 kcal/g. However, because of the energy
expended in converting nitrogen to urea when protein is metabolized
in the body, the energy yield is only about 4.1 kcal/g.
To accurately assess the rate of protein metabolism, the amount of
nitrogen being eliminated from the body must be determined. This
requires urine collection for 12 to 24 h periods, a time-consuming
process. Because the healthy body uses little protein during rest and
exercise (usually not more than 10% of total energy expended),
estimates of total energy expenditure generally ignore protein
metabolism.
TABLE 2.2 ATP Produced From One Molecule of Palmitic Acid
Stage of process
Direct (substrate-level oxidation)
By oxidative phosphorylation
Fatty acid activation
β-oxidation (occurs 7 times)
Krebs cycle (occurs 8 times)
Subtotal
0
0
8
8
−2
28
72
98
Total
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Lactic Acid as a Source of Energy During Exercise
Lactic acid is in a state of constant turnover within cells, being
produced by glycolysis and removed from the cell, primarily through
oxidation. Thus, despite its reputation as a cause of fatigue, lactic
acid can be, and is, used as an actual fuel source during exercise.
This occurs through several mechanisms.
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First, we now know that lactate produced by glycolysis in the
cytoplasm of a muscle fiber can be taken up by the mitochondria
within that same fiber and directly oxidized. This occurs mostly in
cells with a high density of mitochondria like type I (high oxidative)
muscle fibers, cardiac muscle, and liver cells.
Second, lactate produced in a muscle fiber can be transported
away from its site of production and used elsewhere by a process
called the lactate shuttle, first described by Dr. George Brooks.
Lactate is produced primarily by type II muscle fibers but can be
transported to adjacent type I fibers by diffusion or active transport. In
that regard, most of the lactate produced in a muscle never leaves
that muscle. It can also be transported through the circulation to sites
where it can be directly oxidized. The lactate shuttle allows for
glycolysis in one cell to supply fuel for use by another cell. Special
transporters called monocarboxylate transport (MCT) proteins
facilitate the movement of lactate between cells and tissues and likely
within cells. During exercise, approximately 80% to 90% of lactate is
transferred across the sarcolemma either by passive diffusion or by
facilitated transport through MCTs. These transporters can be
expressed in differing numbers, depending on the properties of the
cells and tissues helping to move lactate in the cells that are the most
metabolically active. Using lactate as a metabolic fuel accounts for
approximately 70% to 75% of lactate removal during exercise.
Finally, some of the lactic acid produced in the muscle is
transported by the blood to the liver, where it is reconverted to pyruvic
acid and back to glucose (gluconeogenesis) and transported back to
the working muscle. This is called the Cori cycle. Without this
recycling of lactate into glucose for use as an energy source,
prolonged exercise would be severely limited. On a more integrative
level, lactate produced in exercising skeletal muscle is taken up and
oxidized in the brain. Thus, lactate not only is integrally involved as a
metabolic fuel but also responds to changes in nutrient sensing as
different metabolic fuels are used during exercise.
Summary of Substrate Metabolism
As shown in figure 2.13, the ability to produce muscle contraction for
exercise is a matter of energy supply and energy demand. Both the
contraction of skeletal muscle fibers and their relaxation require
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energy. That energy comes from foodstuffs in the diet and stored
energy in the body. The ATP-PCr system operates within the cytosol
of the cell, as does glycolysis, and neither requires oxygen for ATP
production. Oxidative phosphorylation takes place within the
mitochondria. Note that under aerobic conditions, both major
substrates—carbohydrates and fats—are reduced to the common
intermediate acetyl CoA that enters the Krebs cycle.
RESEARCH PERSPECTIVE 2.2
Lifelong Training Can Lead to More Efficient Fuel
Utilization
While aging is associated with a decrease in exercise capacity and sport
performance, it is clear that the skeletal muscle of older adults can be trained
to meet the demands of exercise. Remaining physically active throughout a
person’s life protects against some of the age-related decrements in musclefiber size, fiber type, mitochondrial number, and oxidative capacity when
compared to older sedentary people. These age-related changes and
adaptations are discussed in greater detail in chapter 18.
A recent study performed at the University of Pittsburgh sought to
determine whether the skeletal muscles of older masters athletes had the
same substrate storage and capacity for oxidation of those fuels as those of
younger athletes who trained similarly (i.e., used the same mode of exercise
and frequency of training).4 That study found that lifelong masters athletes
have greater triglyceride stores in their muscle fibers and a greater proportion
of oxidative fibers compared to the young athletes. These differences resulted
in better metabolic efficiency—a lower reliance on carbohydrate oxidation—
during exercise at high intensities in the older athletes (see figure). Lifelong
endurance exercise protects against some of the age-associated decreases in
oxidative potential and provides older athletes with an increased capacity for
fat oxidation to produce ATP during exercise.
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A simplified illustration of carbohydrate oxidation at different relative exercise
intensities in younger and older adult athletes. Lifelong masters endurance athletes
rely less on carbohydrate oxidation at higher exercise intensities compared to similarly
trained younger athletes.
FIGURE 2.13 The metabolism of carbohydrate, fat, and (to a lesser extent) protein shares some
common pathways within the muscle fiber. The adenosine triphosphate (ATP) molecules generated by
oxidative and nonoxidative metabolism are used by those steps in muscle contraction and relaxation that
demand energy.
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In Review
The oxidative system involves the breakdown of substrates in the presence of
oxygen. This system yields more energy than the ATP-PCr or the glycolytic
system.
Oxidation of carbohydrate involves glycolysis, the Krebs cycle, and the electron
transport chain. The end result is H2O, CO2, and 32 or 33 ATP molecules per
carbohydrate molecule.
Fat oxidation begins with β-oxidation of FFAs and then follows the same path as
carbohydrate oxidation: acetyl CoA moving into the Krebs cycle and the electron
transport chain. The energy yield for fat oxidation is much higher than for
carbohydrate oxidation, and it varies with the FFA being oxidized. However, the
maximum rate of high-energy phosphate formation from lipid oxidation is too low
to match the rate of utilization of high-energy phosphate during higher-intensity
exercise, and the energy yield of fat per oxygen molecule used is much less than
that for carbohydrate.
Although fat provides more kilocalories of energy per gram than carbohydrate, fat
oxidation requires more oxygen than carbohydrate oxidation. The energy yield
from fat is 5.6 ATP molecules per oxygen molecule used, compared with
carbohydrate’s yield of 6.3 ATP per oxygen molecule. Oxygen delivery is limited
by the oxygen transport system, so carbohydrate is the preferred fuel during highintensity exercise.
The maximum rate of ATP production from lipid oxidation is too low to match the
rate of utilization of ATP during high-intensity exercise. This explains the reduction
in an athlete’s race pace when carbohydrate stores are depleted and fat, by
default, becomes the predominant fuel source.
Measurement of protein oxidation is more complex because amino acids contain
nitrogen, which cannot be oxidized. Protein contributes relatively little to energy
production, generally less than 10%, so its metabolism is often considered
negligible.
Despite its reputation as a potential factor in causing fatigue, lactic acid can be,
and is, used as an important fuel source during exercise.
Interaction of the Energy Systems
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The three energy systems do not work independently of one another,
and no activity is 100% supported by any single energy system.
When a person exercises at the highest intensity possible, from the
shortest sprints (less than 10 s) to endurance events (greater than 30
min), each of the energy systems is contributing to the total energy
needs of the body. Generally, one energy system dominates energy
production, except when there is a transition from the predominance
of one energy system to another. As an example, in a 10 s, 100 m
sprint, the ATP-PCr system is the predominant energy system, but
both the anaerobic glycolytic and the oxidative systems provide a
small portion of the energy needed. At the other extreme, in a 30 min,
10,000 m (10,936 yd) run, the oxidative system is predominant, but
both the ATP-PCr and anaerobic glycolytic systems contribute some
energy as well.
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FIGURE 2.14 The various energy systems have a reciprocal relation with respect to (a) the maximal
rate at which energy can be produced and (b) the capacity to produce that energy.
Figure 2.14 shows the reciprocal relation among the energy
systems with respect to power and capacity. The ATP-PCr energy
system can provide energy at a fast rate but has a very low capacity
for energy production. Thus it supports exercise that is intense but of
very short duration. By contrast, fat oxidation takes longer to gear up
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and produces energy at a slower rate; however, the amount of energy
it can produce is unlimited. The characteristics of the muscle fiber’s
energy systems are listed in table 2.3.
The Crossover Concept
The crossover concept was first described by Brooks and Mercier1
to describe the relative balance between carbohydrate (CHO) and fat
metabolism during sustained exercise. At rest and during exercise at
low to moderate intensities (below 60% of maximal oxygen uptake),
lipids serve as the main substrate for generating ATP. During highintensity exercise (above 75% of maximal oxygen uptake), increases
in muscle glycogenolysis and the recruitment of more type II muscle
fibers promote a shift to CHO as the predominant substrate for
generating ATP. The crossover point is the intensity where fat and
carbohydrate utilization intersect (figure 2.15) as the energy from fat
decreases and the energy from carbohydrate increases. Beyond this
crossover point, further increases in power are met with further
increments in CHO utilization and decrements in fat oxidation.
The crossover point is affected by both the exercise intensity and
endurance training status. Endurance training results in biochemical
adaptations within the muscle fibers that promote and support
oxidation of FFAs, including an increase in the number of
mitochondria, increased oxidative enzymes, and changes in βoxidation and the electron transport chain—all important determinants
of fat metabolism. The result of training is to allow the body to spare
muscle glycogen, since carbohydrate stores within the body are
limited. These training-induced adaptations shift the crossover point
toward higher exercise intensities. Diet (energy supply and stores)
and prior exercise play secondary roles in determining the balance of
substrates utilization during submaximal exercise.
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FIGURE 2.15 The relation between the relative contributions of fat and carbohydrate (CHO) utilization
to overall energy expenditure as a function of exercise intensity. The point at which the two lines
intersect illustrates the classic crossover concept.
The Oxidative Capacity of Muscle
We have seen that the processes of oxidative metabolism have the
highest energy yields. It would be ideal if these processes always
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functioned at peak capacity. But, as with all physiological systems,
they operate within certain constraints. The oxidative capacity of
muscle ( O2) is a measure of its maximal capacity to use oxygen.
This measurement is made in the laboratory, where a small amount of
muscle tissue can be tested to determine its capacity to consume
oxygen when chemically stimulated to generate ATP. A muscle’s
oxidative capacity ultimately depends on its oxidative enzyme
concentrations, fiber type composition, and oxygen availability.
Enzyme Activity
The capacity of muscle fibers to oxidize carbohydrate and fat is
difficult to determine. Numerous studies have shown a close relation
between a muscle’s ability to perform prolonged aerobic exercise and
the activity of its oxidative enzymes. Because many different
enzymes are required for oxidation, the enzyme activity of the muscle
fibers provides a reasonable indication of their oxidative potential.
Measuring all the enzymes in muscles is impossible, so a few
representative enzymes have been selected to reflect the aerobic
capacity of the fibers. The enzymes most frequently measured are
succinate dehydrogenase and citrate synthase, mitochondrial
enzymes involved in the Krebs cycle (see figure 2.9). Figure 2.16
illustrates the close correlation between succinate dehydrogenase
activity in the vastus lateralis muscle and that muscle’s oxidative
capacity. Endurance athletes’ muscles have oxidative enzyme
activities two to four times greater than those of untrained men and
women.
Fiber Type Composition and Endurance Training
A muscle’s fiber type composition primarily determines its oxidative
capacity. As noted in chapter 1, type I (slow-twitch) fibers have a
greater capacity for aerobic activity than type II (fast-twitch) fibers
because type I fibers have more mitochondria and higher
concentrations of oxidative enzymes. Type II fibers are better suited
for glycolytic energy production. Thus, in general, the more type I
fibers in one’s muscles, the greater the oxidative capacity of those
muscles. Elite distance runners, for example, possess more type I
fibers, more mitochondria, and higher muscle oxidative enzyme
activities than do untrained individuals.
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FIGURE 2.16 The relation between muscle succinate dehydrogenase (SDH) activity and its oxidative
capacity ( O2), measured in a muscle biopsy sample taken from the vastus lateralis.
Endurance training enhances the oxidative capacity of all fibers,
especially type II fibers. Training that places demands on oxidative
phosphorylation stimulates the muscle fibers to develop more
mitochondria, larger mitochondria, and more oxidative enzymes per
mitochondrion. By increasing the fibers’ enzymes for β-oxidation, this
training also enables the muscle to rely more on fat for aerobic ATP
production. Thus, with endurance training, even people with large
percentages of type II fibers can increase their muscles’ aerobic
capacities. But it is generally agreed that an endurance-trained type II
fiber will not develop the same high endurance capacity as a similarly
trained type I fiber.
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Oxygen Needs
Although the oxidative capacity of a muscle is determined by the
number of mitochondria and the amount of oxidative enzymes
present, oxidative metabolism ultimately depends on an adequate
supply of oxygen. At rest, the need for ATP is relatively small,
requiring minimal oxygen delivery. As exercise intensity increases, so
do energy demands. To meet them, the rate of oxidative ATP
production increases. In an effort to meet the muscles’ need for
oxygen, the rate and depth of respiration increase, improving gas
exchange in the lungs, and the heart beats faster and more forcefully,
pumping more oxygenated blood to the muscles. Arterioles dilate to
facilitate delivery of arterial blood to muscle capillaries.
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The human body stores little oxygen. Therefore, the amount of
oxygen entering the blood as it passes through the lungs is directly
proportional to the amount used by the tissues for oxidative
metabolism. Consequently, a reasonably accurate estimate of aerobic
energy production can be made by measuring the amount of oxygen
consumed at the lungs (see chapter 5).
RESEARCH PERSPECTIVE 2.3
Does the Muscle Fiber’s Oxidative Capacity Determine
Fitness Level?
Maximal oxygen uptake ( O2max; discussed in detail in chapter 5) is a
measurement of cardiorespiratory fitness, so it is not surprising that welltrained endurance athletes have a high O2max. The ability to take in and use
oxygen during aerobic exercise may be limited by any number of factors along
the pathway of the O2 molecule as it moves from the atmosphere to the
mitochondria to be used for energy: pulmonary ventilation, the oxygencarrying capacity of the blood, and blood flow to exercising muscle, to name a
few. Maximal oxygen uptake is also an important predictor of health, and
reductions in O2max are associated with a loss of mobility and independence
in the elderly and an increase in mortality in many chronic diseases. Because
of its critical role, exercise physiologists are keenly interested in the factors
that limit
O2max in all people, from chronic heart failure patients to
professional endurance athletes.
Since the early development of measurement techniques to quantify
O2max in humans, researchers have designed studies to systematically
examine each point along the oxygen delivery pathway from inspired air to the
mitochondria within muscle fibers. Because it is well accepted that increasing
oxygen supply to the working muscle improves O2max and exercise capacity,
many scientists believed that the ability of the mitochondria themselves to use
oxygen—mitochondrial oxidative capacity—was not a limiting factor for
maximal oxygen uptake. However, a recent study examined how well the
mitochondrial oxidative capacity alone was associated with O2max across
people of vastly different fitness levels.8
In that study, researchers measured O2max during cycling exercise in
chronic heart failure patients, healthy subjects, and elite cyclists. They then
took muscle biopsy samples from the quadriceps of each subject to measure
mitochondrial oxidative capacity. To quantify the muscle fibers’ capacity to
utilize oxygen, they measured the activity of an important enzyme in the Krebs
cycle, succinate dehydrogenase. Interestingly, they found that this measure of
mitochondrial oxidative capacity was related to O2max across all subjects,
184
regardless of fitness or health status (see figure). Their results indicated that
while limitations in oxygen supply certainly limit O2max, maximal oxygen
uptake during whole-body exercise is partially determined at the level of the
muscle fiber itself.
Simplified figure showing the relation between mitochondrial oxidative capacity,
measured as succinate dehydrogenase activity in skeletal muscle biopsy samples
obtained from the quadriceps after cycle exercise, and maximal oxygen uptake in
chronic heart failure patients (CHF), healthy adults, and elite cyclists. Maximal oxygen
uptake is closely related to mitochondrial oxidative capacity across all three subject
groups.
185
IN CLOSING
In this chapter, we focused on energy metabolism and the synthesis of the
storage form of energy in the body, ATP. We described in some detail the three
basic energy systems used to generate ATP and their regulation and interaction.
Finally, we highlighted the important role that oxygen plays in the sustained
generation of ATP for continued muscle contraction and the three fiber types
found in human skeletal muscle. We next look at the neural control of exercising
muscle.
KEY TERMS
acetyl coenzyme A (acetyl CoA)
activation energy
adenosine diphosphate (ADP)
aerobic metabolism
anaerobic metabolism
ATP-PCr system
β-oxidation
bioenergetics
carbohydrate
catabolism
creatine kinase
crossover concept
cytochrome
electron transport chain
enzyme
free fatty acids (FFAs)
gluconeogenesis
glucose
glycogen
glycogenolysis
glycolysis
kilocalories (kcal)
Krebs cycle
lipogenesis
lipolysis
metabolism
mitochondria
negative feedback
oxidative phosphorylation
186
oxidative system
phosphocreatine (PCr)
phosphofructokinase (PFK)
phosphorylation
rate-limiting enzyme
substrate
triglycerides
STUDY QUESTIONS
1.
What is ATP, how is it formed, and how does it provide energy during
metabolism?
2.
What is the primary substrate used to provide energy at rest? During highintensity exercise?
3.
What is the role of PCr in energy production, and what are its limitations?
Describe the relationship between muscle ATP and PCr during sprint
exercise.
4.
5.
6.
7.
Describe the essential characteristics of the three energy systems.
8.
9.
What is lactic acid, and why is it important?
Why are the ATP-PCr and glycolytic energy systems considered anaerobic?
What role does oxygen play in the process of aerobic metabolism?
Describe the by-products of energy production from ATP-PCr, glycolysis,
and oxidation.
Discuss the interaction among the three energy systems with respect to the
rate at which energy can be produced and the sustained capacity to
produce that energy.
10.
What is meant by the crossover concept, and how does it change with
endurance exercise training?
11.
How do type I muscle fibers differ from type II fibers in their respective
oxidative capacities? What accounts for those differences?
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
187
188
3
Neural Control of Exercising Muscle
In this chapter and in the web study guide
Structure and Function of the Nervous System
Neuron
Nerve Impulse
Synapse
Neuromuscular Junction
Neurotransmitters
Postsynaptic Response
ACTIVITY 3.1 The Neuron reviews the basic structure of a neuron.
AUDIO FOR FIGURE 3.3 describes the voltage and ion permeability changes during an action
potential.
ACTIVITY 3.2 Action Potentials explores the sequence of events that occur during an action potential.
ACTIVITY 3.3 Communication Among Components explores the way that neurons and muscle fibers
communicate.
Central Nervous System
Brain
Spinal Cord
ACTIVITY 3.4 Central Nervous System describes the components of the central nervous system.
ACTIVITY 3.5 Higher Brain Center Function reviews the functions of the higher brain centers.
Peripheral Nervous System
Sensory Division
Motor Division
Autonomic Nervous System
ACTIVITY 3.6 Peripheral Nervous System identifies the functions and components of the peripheral
nervous system.
Sensory-Motor Integration
Sensory Input
189
Motor Response
ANIMATION FOR FIGURE 3.7 shows the steps in the process of sensory-motor integration.
AUDIO FOR FIGURE 3.8 describes the pathways of sensory receptors.
AUDIO FOR FIGURE 3.9 describes the structure of a muscle spindle and Golgi tendon organ.
In Closing
190
J
osh Harding retired from the National Hockey League (NHL) in 2015 after an
8-year career as a goalie, posting 60 NHL wins. While warming up for a game,
Harding felt a tweak in his neck, followed by dizziness, black spots in front of his
eyes, and numbness in his right leg. In December of 2012, just before the 20122013 NHL season began, Harding learned he had multiple sclerosis (MS), a
disease that attacks the central nervous system and causes a loss of balance and
coordination, blurred vision, dehydration, muscle spasms, and weakness. His team,
the Minnesota Wild, was made aware of the diagnosis, and Harding eventually
made the news public. Despite the challenges that this diagnosis imposes on an
NHL goaltender, Harding was determined to continue to play, and play well he did
for a while. However, after playing two periods for the minor-league Iowa Wild in
2014, Harding was taken by ambulance to the hospital suffering from severe
dehydration, a common effect of MS. In his first full season after being diagnosed,
he played 29 games with an 18-7-3 record, a 1.65 goals against average, and a
0.933 save percentage. Harding received the Bill Masterson Memorial Trophy in
recognition of his perseverance and dedication to the game. Having found the
correct combination of medication and a sleep schedule that works, he now serves
as a high school goaltender coach while raising three young children.
All functions within the human body are influenced in some way by
the nervous system. Nerves are the wiring through which electrical
impulses are sent to and received from virtually all tissues of the
body. The brain acts as a central computer, integrating incoming
information, selecting an appropriate response, and then signaling
the involved organs and tissues to take appropriate action. Thus, the
nervous system forms a vital network, allowing communication,
coordination, and interaction of the various tissues and systems in
the body as well as between the body and the external environment.
The nervous system is one of the body’s most complex systems.
Because this book is primarily concerned with neural control of
muscle contraction and voluntary movement, we will limit our
coverage of this complex system. We first review the structure and
function of the nervous system and then focus on specific topics
relevant to sport and exercise.
Before we examine the intricate details of the nervous system, it is
important to look at how the nervous system is organized and how
191
that organization functions to integrate and control movement. The
nervous system is commonly divided into two parts: the central
nervous system (CNS) and the peripheral nervous system
(PNS). The CNS is composed of the brain and spinal cord, while the
PNS is further divided into sensory (afferent) nerves and effector
(efferent) nerves. Sensory nerves are responsible for informing the
CNS about what is going on within and outside the body. Efferent
nerves are responsible for sending information from the CNS to the
various tissues, organs, and systems of the body in response to the
signals coming in from the sensory division. The term motor neuron
(motor nerve) classically applies to neurons that project their axons
outside the CNS to directly or indirectly control muscles. The efferent
nervous system is composed of two parts, the autonomic nervous
system and the somatic nervous system. Figure 3.1 provides a
schematic of these relationships. More detail concerning each of
these individual units of the nervous system is presented later in this
chapter.
FIGURE 3.1 Organization of the nervous system.
Structure and Function of the Nervous System
The neuron is the basic structural unit of the nervous system. We
first review the anatomy of the neuron and then look at how it
192
functions—allowing electrical impulses to be transmitted throughout
the body.
Neuron
Individual nerve fibers (nerve cells), depicted in figure 3.2, are called
neurons. A typical neuron is composed of three regions:
The cell body, or soma
The dendrites
The axon
FIGURE 3.2 A drawing and photomicrograph (inset) of a neuron and its structure.
The cell body contains the nucleus. Radiating out from the cell
body are the two cell processes: dendrites and the axon. On the side
toward the axon, the cell body tapers into a cone-shaped region
known as the axon hillock. The axon hillock has an important role in
impulse conduction, as discussed later.
Most neurons contain only one axon but many dendrites.
Dendrites are the neuron’s receivers. Most impulses, or action
potentials, that enter the neuron from sensory stimuli or from
adjacent neurons typically enter the neuron via the dendrites. These
processes then carry the impulses toward the cell body.
193
The axon is the neuron’s transmitter and conducts impulses away
from the cell body. Near its end, an axon splits into numerous end
branches. The tips of these branches are dilated into tiny bulbs
known as axon terminals or synaptic knobs. These terminals or
knobs house numerous vesicles (sacs) filled with chemicals known
as neurotransmitters that are used for communication between a
neuron and another cell. (This is discussed in more detail later in the
chapter.) The structure of the neuron allows nerve impulses to enter
the neuron through the dendrites, and to a lesser extent through the
cell body, and to travel through the cell body and axon hillock, down
the axon, and out through the end branches to the axon terminals.
We next look in more detail at how this happens, including how
these impulses travel from one neuron to another and from a
somatic motor neuron to muscle fibers.
Nerve Impulse
Neurons are referred to as excitable tissue because they can
respond to various types of stimuli and convert those messages to
an electrical signal called a nerve impulse. A nerve impulse arises
when a stimulus is strong enough to substantially change the normal
electrical charge of the neuron. That signal then moves along the
neuron down the axon and toward an end organ, such as another
neuron or a group of muscle fibers. A useful analogy is between the
nerve impulse traveling through a neuron and electricity traveling
through the electrical wires in a home. This section describes how
the electrical impulse is generated and how it travels through a
neuron.
Resting Membrane Potential
The cell membrane of a typical neuron at rest has a negative
electrical potential of about −70 mV. This means that if one were to
insert a voltmeter probe inside the cell, the electrical charges found
there and the charges found outside the cell would differ by 70 mV,
and the inside would be negative relative to the outside. This
electrical potential difference is known as the resting membrane
potential (RMP). It is caused by an uneven separation of charged
ions across the membrane. When the charges across the membrane
differ, the membrane is said to be polarized.
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The neuron has a high concentration of potassium ions (K+) on
the inside of the membrane and a high concentration of sodium ions
(Na+) on the outside. The imbalance in the number of ions inside and
outside the cell causes the RMP. This imbalance is maintained in two
ways. First, the cell membrane is much more permeable to K+ than
to Na+, so the K+ can move more freely. Because ions tend to move
to establish equilibrium, some of the K+ will move to the area where
they are less concentrated, outside the cell. The Na+ cannot move to
the inside as easily. Second, sodium–potassium pumps in the
neuron membrane, which contain Na+-K+ adenosine triphosphatase
(Na+-K+-ATPase), maintain the imbalance on each side of the
membrane by actively transporting potassium ions in and sodium
ions out. The sodium–potassium pump moves three Na+ out of the
cell for each two K+ it brings in. The end result is that more positively
charged ions are outside the cell than inside, creating the potential
difference across the membrane. Maintenance of a constant RMP of
about −70 mV is primarily a function of the sodium–potassium pump.
Depolarization and Hyperpolarization
If the inside of the cell becomes less negative relative to the outside,
the potential difference across the membrane decreases. The
membrane will be less polarized. When this happens, the membrane
is said to be depolarized. Thus, depolarization occurs any time the
charge difference becomes more positive than the RMP of −70 mV,
moving closer to zero. This typically results from a change in the
membrane’s Na+ permeability.
The opposite can also occur. If the charge difference across the
membrane increases, moving from the RMP to an even more
negative value, then the membrane becomes more polarized. This is
known as hyperpolarization. Changes in the membrane potential
control the signals used to receive, transmit, and integrate
information within and between cells. These signals are of two types,
graded potentials and action potentials. Both are electrical currents
created by the movement of ions.
Graded Potentials
Graded potentials are localized changes in the membrane
potential, either depolarization or hyperpolarization. The membrane
195
contains ion channels with gates that act as doorways into and out of
the neuron. These gates are usually closed, preventing a large
number of ions from flowing into and out of the membrane—that is,
above and beyond the constant movement of Na+ and K+ that
maintains the RMP. However, with potent enough stimulation, the
gates open, allowing more ions to move from the outside to the
inside or vice versa. This ion flow alters the charge separation,
changing the polarization of the membrane.
Graded potentials are triggered by a change in the neuron’s local
environment. Depending on the location and type of neuron involved,
the ion gates may open in response to the transmission of an
impulse from another neuron or in response to sensory stimuli such
as changes in chemical concentrations, temperature, or pressure.
Recall that most neuron receptors are located on the dendrites
(although some are on the cell body), yet the impulse is always
transmitted from the axon terminals at the opposite end of the cell.
For a neuron to transmit an impulse, the impulse must travel almost
the entire length of the neuron. Although a graded potential may
result in depolarization of the entire cell membrane, it is usually just a
local event such that the depolarization does not spread very far
along the neuron. To travel the full distance, an impulse must be
sufficiently strong to generate an action potential.
Action Potentials
An action potential is a rapid and substantial depolarization of the
neuron’s membrane. It usually lasts only about 1 ms. Typically, the
membrane potential changes from the RMP of about −70 mV to a
value of about +30 mV and then rapidly returns to its resting value.
This is illustrated in figure 3.3. How does this marked change in
membrane potential occur?
All action potentials begin as graded potentials. When enough
stimulation occurs to cause a depolarization of at least 15 to 20 mV,
an action potential results. In other words, if the membrane
depolarizes from the RMP of −70 mV to a value of −50 to −55 mV,
an action potential will occur. The membrane voltage at which a
graded potential becomes an action potential is called the
depolarization threshold. Any depolarization that does not attain the
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threshold will not result in an action potential. For example, if the
membrane potential changes from the RMP of −70 mV to −60 mV,
the change is only 10 mV and does not reach the threshold; thus, no
action potential occurs. But any time depolarization reaches or
exceeds the threshold, an action potential will result. This is
commonly referred to as the all-or-none principle.
FIGURE 3.3 Voltage and ion permeability changes during an action potential.
When a segment of an axon’s sodium gates is open and it is in
the process of generating an action potential, it is unable to respond
to another stimulus. This is referred to as the absolute refractory
period. When the sodium gates are closed, the potassium gates are
open, and repolarization is occurring, that segment of the axon can
potentially respond to a new stimulus, but the stimulus must be of
substantially greater magnitude to evoke an action potential. This is
referred to as the relative refractory period.
Propagation of the Action Potential
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Now that we understand how a neural impulse, in the form of an
action potential, is generated, we can look at how the impulse is
propagated—that is, how it travels through the neuron. Two
characteristics of the neuron determine how quickly an impulse can
pass along the axon: myelination and diameter.
The axons of many neurons, especially large neurons,
are myelinated, meaning that they are covered with a sheath formed
by myelin, a fatty substance that insulates the cell membrane. This
myelin sheath (see figure 3.2) is formed by specialized cells called
Schwann cells.
The myelin sheath is not continuous. As it spans the length of the
axon, the myelin sheath has gaps between adjacent Schwann cells,
leaving the axon uninsulated at those points. These gaps are
referred to as nodes of Ranvier (see figure 3.2). The action potential
appears to jump from one node to the next as it traverses a
myelinated fiber. This is referred to as saltatory conduction, a
much faster type of conduction than occurs in unmyelinated fibers.
Myelination of peripheral motor neurons occurs over the first
several years of life, partly explaining why children need time to
develop coordinated movement. Individuals affected by certain
neurological diseases (such as multiple sclerosis, as discussed in
our chapter opening) experience degeneration of the myelin sheath
and a subsequent loss of coordination.
Myelination
The velocity of nerve impulse transmission is
also determined by the neuron’s size. Neurons of larger diameter
conduct nerve impulses faster than neurons of smaller diameter
because larger neurons present less resistance to local current flow.
Diameter of the Neuron
In Review
Neurons are excitable tissues because they have the ability to respond to various
types of stimuli and convert them to an electrical signal or nerve impulse.
A neuron’s RMP of about −70 mV results from the unequal separation of
positively charged sodium and potassium ions, with more potassium inside the
membrane and more sodium on the outside.
The RMP is maintained by actions of the sodium–potassium pump, coupled with
low sodium permeability and high potassium permeability of the neuron
198
membrane.
Any change that makes the membrane potential less negative results in
depolarization. Any change making this potential more negative is a
hyperpolarization. These changes occur when ion gates in the membrane open,
permitting more ions to move across the membrane.
If the membrane is depolarized by 15 to 20 mV, the depolarization threshold is
reached and an action potential results. Action potentials are not generated if the
threshold is not met.
In myelinated neurons, the impulse travels through the axon by jumping between
nodes of Ranvier (gaps between the cells that form the myelin sheath). This
process, saltatory conduction, results in nerve transmission rates 5 to 50 times
faster than in unmyelinated fibers of the same size. Impulses also travel faster in
neurons of larger diameter.
Synapse
For a neuron to communicate with another neuron, an action
potential must occur and travel along the first neuron, ultimately
reaching its axon terminals. How does the action potential then move
from the neuron in which it starts to another neuron to continue
transmitting the electrical signal?
Neurons communicate with each other across junctions called
synapses. A synapse is the site of action potential transmission from
the axon terminals of one neuron to the dendrites or soma of
another. There are both chemical and mechanical synapses, but the
most common type is the chemical synapse, which is our focus. It is
important to note that the signal that is transmitted from one neuron
to another changes from electrical to chemical, then back to
electrical.
199
FIGURE 3.4 A chemical synapse between two neurons, showing the synaptic vesicles containing
neurotransmitter molecules.
As seen in figure 3.4, a synapse between two neurons includes
the axon terminals of the neuron sending the action potential,
receptors on the neuron receiving the action potential, and
the space between these structures.
The neuron sending the action potential across the synapse is
called the presynaptic neuron, so axon terminals are presynaptic
terminals. Similarly, the neuron receiving the action potential on the
opposite side of the synapse is called the postsynaptic neuron, and it
has postsynaptic receptors. The axon terminals and postsynaptic
receptors are not physically in contact with each other. A narrow gap,
the synaptic cleft, separates them.
The action potential can be transmitted across a synapse in only
one direction: from the axon terminal of the presynaptic neuron to
the postsynaptic receptors, about 80% to 95% of which are on the
dendrites of the postsynaptic neuron. The remaining 5% to 20% of
the postsynaptic receptors are adjacent to the cell body instead of
being located on the dendrites. Why can the action potential go in
only one direction?
The presynaptic terminals of the axon contain a large number of
saclike structures called synaptic (or storage) vesicles. These
vesicles contain a variety of chemical compounds called
200
neurotransmitters because they function to transmit the neural signal
to the next neuron. When the impulse reaches the presynaptic axon
terminals, the synaptic vesicles respond by releasing the
neurotransmitters into the synaptic cleft. These neurotransmitters
then diffuse across the synaptic cleft to the postsynaptic neuron’s
receptors. Each neurotransmitter then binds to its specialized
postsynaptic receptors. When sufficient binding occurs, a series of
graded depolarizations occurs. If the depolarization reaches the
threshold, an action potential occurs, and the impulse has been
transmitted successfully to the next neuron. Depolarization of the
second nerve depends on both the amount of neurotransmitter
released and the number of available receptor binding sites on the
postsynaptic neuron.
Neuromuscular Junction
Recall from chapter 1 that a single α-motor neuron and all of the
muscle fibers it innervates is called a motor unit. Whereas neurons
communicate with other neurons at synapses, an α-motor neuron
communicates with its muscle fibers at a site known as a
neuromuscular junction, which functions in essentially the same
manner as a synapse. In fact, the proximal part of the neuromuscular
junction is the same: It starts with the axon terminals of the motor
neuron, which release neurotransmitters into the space between the
motor nerve and the muscle fiber in response to an action potential.
However, in the neuromuscular junction, the axon terminals protrude
into motor end plates, which are invaginated (folded to form cavities)
segments on the plasmalemma of the muscle fiber (see figure 3.5).
FIGURE 3.5 The neuromuscular junction, illustrating the interaction between the
the plasmalemma of a single muscle fiber.
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α-motor neuron and
Neurotransmitters—primarily acetylcholine (ACh)— released from
the α-motor neuron axon terminals diffuse across the synaptic cleft
and bind to receptors on the muscle fiber’s plasmalemma. This
binding typically causes depolarization by opening sodium ion
channels, allowing more sodium to enter the muscle fiber. Again, if
the depolarization reaches the threshold, an action potential is
formed. It spreads across the plasmalemma into the T-tubules,
initiating muscle fiber contraction. As in the neuron, the
plasmalemma, once depolarized, must undergo repolarization.
During the period of repolarization, the sodium gates are closed and
the potassium gates are open; thus, like the neuron, the muscle fiber
is unable to respond to any further stimulation during this refractory
period. Once the RMP of the muscle fiber is restored, the fiber can
respond to another stimulus. Thus, the refractory period limits the
motor unit’s firing frequency.
Exercise training induces changes not only in skeletal muscle, but
also at the neuromuscular junction (NMJ) to increase presynaptic
release of, and sensitivity of the muscle cell to, acetylcholine. These
changes occur through a number of different cellular signaling
mechanisms; however, many of the changes induced by training
share a common signaling molecule, the peroxisome proliferator–
activated receptor-γ coactivator 1α(PGC-1α). PGC-1α contributes to
the remodeling of the NMJ in several ways. First, PGC-1α induces
adaptations in the motor neuron itself by increasing branching of the
presynaptic terminal motor neuron and increasing the number of
presynaptic vesicles containing acetylcholine. Second, PGC-1α
increases the number of acetylcholine receptors on the cell
membrane, thus amplifying the effects for a given amount of
acetylcholine released from the motor neuron.4 Finally, PGC-1α is
involved in decreasing the size of the motor end plate (i.e., fewer
fibers per motor unit) on glycolytic fibers, making them similar to
more oxidative fibers.
Muscular fatigue (discussed in detail in chapter 5) is a complex
phenomenon, with many possible contributing factors. One
mechanism that may contribute to muscle fatigue is a decline in
signal transmission through the NMJ. Prior exercise can decrease
202
motor nerve outflow and neuromuscular transmission rates,3 which
leads to decreased force production.
Now we know how the impulse is transmitted from nerve to nerve
or nerve to muscle. But to understand what happens once the
impulse is transmitted, we must first examine the chemical signaling
molecules, the neurotransmitters, that accomplish this signal
transmission.
Neurotransmitters
More than 50 neurotransmitters have been positively identified or are
suspected to be potential candidates. These can be categorized as
either (a) small-molecule, rapid-acting neurotransmitters or (b)
neuropeptide, slow-acting neurotransmitters. The small-molecule,
rapid-acting transmitters, which are responsible for most neural
transmissions, are our main focus.
RESEARCH PERSPECTIVE 3.1
Motor Units Adapt to High-Intensity Interval Training
High-intensity interval training (HIIT, discussed in chapter 11) is a mode of
physical activity that involves brief, intermittent bursts of vigorous activity
interspersed with periods of low-intensity exercise or rest. An individual can
reap the same cardiovascular and musculoskeletal benefits from exercise
training using HIIT in far less time compared to traditional long-duration
endurance training (END). Because HIIT is now a common alternative to
END and exercise training changes the neural control of muscle function, it is
important to systematically evaluate HIIT-induced neuromuscular
adaptations.
High-density surface electromyography (EMG) is a relatively new
technological advancement that allows for both the simultaneous assessment
of several motor units over a wide range of forces and the ability to track the
same motor units during different sessions over a long period of time (like
during exercise training). Recording motor unit activity and function allows
investigators to assess the way the nervous system controls muscle force.
Researchers recently evaluated differences in the neuromuscular adaptations
to HIIT and END using this technique.6 Two weeks of HIIT and END elicited
similar improvements in cardiorespiratory fitness, but there were distinct
adjustments in motor unit behavior with the two types of training. HIIT
increased both maximum force production and motor unit discharge. In
contrast, END did not influence motor unit firing. These findings suggest that
HIIT and END have very different effects on motor unit function and provide
203
important
new
information
regarding
exercise
training–induced
neuromuscular adaptations. This study was also the first to demonstrate
training-induced changes in motor unit discharge rate by tracking the same
individual motor units before and after training. This innovative methodology
will likely continue to broaden our understanding of neural adaptations to
exercise training.
Acetylcholine and norepinephrine are the two major
neurotransmitters involved in regulating multiple physiological
responses
to
exercise.
Acetylcholine
is
the
primary
neurotransmitter for the motor neurons that innervate skeletal
muscle as well as for most parasympathetic autonomic neurons. It is
generally an excitatory neurotransmitter in the somatic nervous
system but can have inhibitory effects at some parasympathetic
nerve endings, such as in the heart. Norepinephrine is the
neurotransmitter for most sympathetic autonomic neurons, and it too
can be either excitatory or inhibitory, depending on the receptors
involved. Nerves that primarily release norepinephrine are called
adrenergic, and those that have acetylcholine as their primary
neurotransmitter are termed cholinergic. Two major subtypes of
cholinergic receptors are muscarinic and nicotinic, with the former
involved in motor nerve transmission. The sympathetic and
parasympathetic branches of the autonomic nervous systems are
discussed later in this chapter.
Once the neurotransmitter binds to the postsynaptic receptor, the
nerve impulse has been successfully transmitted. The
neurotransmitter then (1) is degraded by enzymes, (2) is actively
transported back into the presynaptic terminals for reuse, or (3)
diffuses away from the synapse.
In Review
Neurons communicate with each other across synapses composed of the axon
terminals of the presynaptic neuron, the postsynaptic receptors on the dendrite
or cell body of the postsynaptic neuron, and the synaptic cleft between the two
neurons.
A nerve impulse causes neurotransmitters to be released from the presynaptic
axon terminal into the synaptic cleft.
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Neurotransmitters diffuse across the cleft and bind to the postsynaptic receptors.
Once sufficient neurotransmitters are bound, the impulse is successfully
transmitted and the neurotransmitter is then destroyed by enzymes, is removed
by reuptake into the presynaptic terminal for future use, or diffuses away from the
synapse.
Neurotransmitter binding at the postsynaptic receptors opens ion gates in the
given membrane and can cause depolarization (excitation) or hyperpolarization
(inhibition), depending on the specific neurotransmitter and the receptors to
which it binds.
Neurons communicate with muscle fibers at neuromuscular junctions. A
neuromuscular junction involves presynaptic axon terminals, the synaptic cleft,
and motor end-plate receptors on the plasmalemma of the muscle fiber and
functions much like a neural synapse.
The neurotransmitters most important in regulating exercise responses are
acetylcholine in the somatic nervous system and norepinephrine in the
autonomic nervous system.
Receptors on the motor end plates of the neuromuscular junction are a special
subtype of cholinergic receptors called muscarinic receptors. They bind the
primary neurotransmitter involved in excitation of muscle fibers, acetylcholine.
Postsynaptic Response
Once the neurotransmitter binds to the receptors, the chemical
signal that traversed the synaptic cleft once again becomes an
electrical signal. The binding causes a graded potential in the
postsynaptic membrane. An incoming impulse may be either
excitatory or inhibitory. An excitatory impulse causes depolarization,
known as an excitatory postsynaptic potential (EPSP). An
inhibitory impulse causes a hyperpolarization, known as an
inhibitory postsynaptic potential (IPSP).
The discharge of a single presynaptic terminal generally changes
the postsynaptic potential less than 1 mV. Clearly this is not sufficient
to generate an action potential, because reaching the threshold
requires a change of at least 15 mV. But when a neuron transmits an
impulse, several presynaptic terminals typically release their
neurotransmitters so that they can diffuse to the postsynaptic
receptors. Also, presynaptic terminals from numerous axons can
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converge on the dendrites and cell body of a single neuron. When
multiple presynaptic terminals discharge at the same time, or when
only a few fire in rapid succession, more neurotransmitter is
released. With an excitatory neurotransmitter, the more that is
bound, the greater the EPSP and the more likely it is that an action
potential will result.
In Review
Excitatory postsynaptic potentials are graded depolarizations of the postsynaptic
membrane; IPSPs are hyperpolarizations of that membrane.
A single presynaptic terminal cannot generate enough of a depolarization to fire
an action potential. Multiple signals are needed. These may come from
numerous neurons or from a single neuron when numerous axon terminals
release neurotransmitters repeatedly and rapidly.
The axon hillock keeps a running total of all EPSPs and IPSPs. When their sum
meets or exceeds the threshold for depolarization, an action potential occurs.
This process of accumulating incoming signals is known as summation.
Summation refers to the cumulative effect of all individual graded potentials as
processed by the axon hillock. Once the sum of all individual graded potentials
meets or exceeds the depolarization threshold, an action potential occurs.
Triggering an action potential at the postsynaptic neuron depends
on the combined effects of all incoming impulses from these various
presynaptic terminals. A number of impulses are needed to cause
sufficient depolarization to generate an action potential. Specifically,
the sum of all changes in the membrane potential must equal or
exceed the threshold. This accumulation of the individual impulses’
effects is called summation.
RESEARCH PERSPECTIVE 3.2
Aging Reduces Rapid Strength
By 2030, it is anticipated that older adults (>65 years) will make up 20% of
the total population. Unfortunately, a large percentage of older adults
experience functional limitations in their activities of daily living, and one out
of three older adults experiences a fall each year. Accidental falls often cause
an accelerated deterioration in overall health and impart a significant
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economic burden on society. Alterations in neuromuscular function have
been suggested to contribute to the increased fall risk in older adults.
Although reduced maximal muscle strength is a well-understood
characteristic of aging, recent studies have demonstrated that rapid strength
(the rate of torque development, or RTD) actually decreases at a greater rate
than maximal strength. Furthermore, RTD measured within the initial 200 ms
from the onset of muscle contraction is more functionally relevant than the
peak torque that can be produced by the muscle. Despite this knowledge,
until recently, no research has specifically targeted the neural and musclespecific factors that contribute to the reductions in RTD with aging. This is a
clinically relevant topic, since this information may help identify strategies to
slow age-related reductions in function, thus reducing the risk of fall-related
injuries.
A group of researchers recently sought to determine the mechanisms of
age-related reductions in RTD.2 Young (20 years old) and older men (70
years old) participated in a study that involved ultrasound assessments of
muscle properties and measurements of muscle strength during early (the
first 50 ms) and late (100 to 200 ms) intervals following the onset of muscle
contraction. RTD was reduced in the older men during the late interval of
contraction, but surprisingly there were no differences in RTD between young
and older men during the early interval of contraction. This suggests that
older men have similar initial muscle activation but are unable to sustain the
same rates of muscle activation during later muscle contraction. Poorer
muscle quality and reductions in pennation angle also contribute to agerelated reductions in RTD, likely because they affect muscle fiber shortening
and fiber rotation. These age-related alterations in neuromuscular function
combine to reduce rapid muscle strength, significantly decreasing
neuromuscular function and contributing to falls in older adults.
For summation, the postsynaptic neuron must keep a running total
of the neuron’s responses, both EPSPs and IPSPs, to all incoming
impulses. This task is done at the axon hillock, which lies on the
axon just past the cell body. Only when the sum of all individual
graded potentials meets or exceeds the threshold can an action
potential occur.
Individual neurons are grouped together into bundles. In the CNS
(brain and spinal cord), these bundles are referred to as tracts, or
pathways. Neuron bundles in the PNS are referred to simply as
nerves.
Central Nervous System
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To comprehend how even the most basic stimulus can cause muscle
activity, we next consider the complexity of the CNS. The CNS
comprises more than 100 billion neurons. In this section, we present
an overview of the components of the CNS and their functions.
Brain
The brain is a highly complex organ composed of numerous
specialized areas. For our purposes, we subdivide it into the four
major regions illustrated in figure 3.6: the cerebrum, diencephalon,
cerebellum, and brain stem.
Cerebrum
The cerebrum is composed of the right and left cerebral
hemispheres. These are connected to each other by the corpus
callosum, fiber bundles (tracts) that allow the two hemispheres to
communicate with each other. The cerebral cortex forms the outer
portion of the cerebral hemispheres and has been referred to as the
site of the mind and intellect. It is also called the gray matter, which
simply reflects its distinctive color resulting from lack of myelin on the
neurons located in this area. The cerebral cortex is the conscious
brain. It allows people to think, be aware of sensory stimuli, and
voluntarily control their movements.
The cerebrum consists of five lobes—four outer lobes and the
central insular lobe—having the following general functions (see
figure 3.6):
Frontal lobe: general intellect and motor control
Temporal lobe: auditory input and interpretation
Parietal lobe: general sensory input and interpretation
Occipital lobe: visual input and interpretation
Insular lobe: diverse functions usually linked to emotion and
self-perception
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FIGURE 3.6 Four major regions of the brain and four outer lobes of the cerebrum. (Note that the
insular lobe is not shown because it is folded deep within the cerebrum between the temporal lobe and
the frontal lobe.)
The three areas in the cerebrum that are of primary concern to
exercise physiology are the primary motor cortex, located in the
frontal lobe; the basal ganglia, located in the white matter below the
cerebral cortex; and the primary sensory cortex, located in the
parietal lobe. In this section, the focus is on the primary motor cortex
and basal ganglia, which work to control and coordinate movement.
The primary motor cortex is responsible for the
control of fine and discrete muscle movements. It is located in the
frontal lobe, specifically within the precentral gyrus. Neurons here,
known as pyramidal cells, let us consciously control movement of
skeletal muscles. Think of the primary motor cortex as the part of the
brain where decisions are made about what movement one wants to
make. For example, in baseball, if a player is in the batter’s box
waiting for the next pitch, the decision to swing the bat is made in the
primary motor cortex, where the entire body is carefully mapped out.
The areas that require the finest motor control have a greater
representation in the motor cortex; thus, more neural control is
provided to them.
Primary Motor Cortex
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The cell bodies of the pyramidal cells are housed in the primary
motor cortex, and their axons form the extrapyramidal tracts. These
are also known as the corticospinal tracts because the nerve
processes extend from the cerebral cortex down to the spinal cord.
These tracts provide the major voluntary control of skeletal muscles.
In addition to the primary motor cortex, there is a premotor cortex
just anterior to the precentral gyrus in the frontal lobe. Learned motor
skills of a repetitious or patterned nature are stored here. This region
can be thought of as the memory bank for skilled motor activities.5
The basal ganglia (nuclei) are not part of the cerebral
cortex. Rather, they are in the cerebral white matter, deep in the
cortex. These ganglia are clusters of nerve cell bodies. The complex
functions of the basal ganglia are not well understood, but the
ganglia are known to be important in initiating movements of a
sustained and repetitive nature (such as arm swinging during
walking), and thus they control complex movements such as walking
and running. These cells also are involved in maintaining posture
and muscle tone.
Basal Ganglia
Diencephalon
The region of the brain known as the diencephalon (see figure 3.6)
contains the thalamus and the hypothalamus. The thalamus is an
important sensory integration center. All sensory input (except smell)
enters the thalamus and is relayed to the appropriate area of the
cortex. The thalamus regulates what sensory input reaches the
conscious brain and thus is very important for motor control.
The hypothalamus, directly below the thalamus, is responsible for
maintaining homeostasis by regulating almost all processes that
affect the body’s internal environment. Neural centers here assist in
the regulation of most physiological systems, including
blood pressure, heart rate, and contractility;
respiration;
digestion;
body temperature;
thirst and fluid balance;
neuroendocrine control;
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appetite and food intake; and
sleep–wake cycles.
Cerebellum
The cerebellum is located behind the brain stem. It is connected to
numerous parts of the brain and has a crucial role in coordinating
movement.
The cerebellum is crucial to the control of all rapid and complex
muscular activities. It helps coordinate the timing of motor activities
and the rapid progression from one movement to the next by
monitoring and making corrective adjustments in the motor activities
that are elicited by other parts of the brain. The cerebellum assists
the functions of both the primary motor cortex and the basal ganglia.
It facilitates movement patterns by smoothing out the movement,
which would otherwise be jerky and uncontrolled.
The cerebellum acts as an integration system, comparing the
programmed or intended activity with the actual changes occurring in
the body and then initiating corrective adjustments through the motor
system. It receives information from the cerebrum and other parts of
the brain and also from sensory receptors (proprioceptors) in the
muscles and joints that keep the cerebellum informed about the
body’s current position. The cerebellum also receives visual and
equilibrium input. Thus, it notes all incoming information about the
exact tension and position of all muscles, joints, and tendons and the
body’s current position relative to its surroundings, then it determines
the best plan of action to produce the desired movement.
After the primary motor cortex makes the decision to perform a
movement, this decision is relayed to the cerebellum. The
cerebellum notes the desired action and then compares the intended
movement with the actual movement based on sensory feedback
from the muscles and joints. If the action is different than planned,
the cerebellum informs the higher centers of the discrepancy so
corrective action can be initiated.
Brain Stem
The brain stem, composed of the midbrain, the pons, and the
medulla oblongata (see figure 3.6), connects the brain and the spinal
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cord. Sensory and motor neurons pass through the brain stem as
they relay information in both directions between the brain and the
spinal cord. This is the site of origin for 10 of the 12 pairs of cranial
nerves. The brain stem also contains the major autonomic centers
that control the respiratory and cardiovascular systems.
A specialized collection of neurons in the brain stem, known as
the reticular formation, is influenced by, and has an influence on,
nearly all areas of the CNS. These neurons help
coordinate skeletal muscle function,
maintain muscle tone,
control cardiovascular and respiratory functions, and
determine state of consciousness (arousal and sleep).
The brain has a pain control system located in the reticular
formation, a group of nerve fibers in the brain stem. Opioid
substances such as enkephalins and β-endorphin act on the opiate
receptors in this region to help modulate pain. Research has
demonstrated that exercise of long duration increases the
concentrations of these substances. While this has been interpreted
as the mechanism causing the “endorphin calm” or “runner’s high”
experienced by some exercisers, the cause–effect association
between endogenous opioids and these sensations has not been
substantiated.
Spinal Cord
The lowest part of the brain stem, the medulla oblongata, is
continuous with the spinal cord below it. The spinal cord is
composed of tracts of nerve fibers that allow two-way conduction of
nerve impulses. The sensory (afferent) fibers carry neural signals
from sensory receptors, such as those in the skin, muscles, and
joints, to the upper levels of the CNS. Motor (efferent) fibers from the
brain and upper spinal cord transmit action potentials to end organs
(e.g., muscles, glands).
In Review
The CNS includes the brain and the spinal cord.
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The four major divisions of the brain are the cerebrum, the diencephalon, the
cerebellum, and the brain stem.
The cerebral cortex is the conscious brain. The primary motor cortex, located in
the frontal lobe, is the center of conscious motor control.
The basal ganglia, in the cerebral white matter, help initiate some movements
(sustained and repetitive ones) and help control posture and muscle tone.
The diencephalon includes the thalamus, which receives all sensory input
entering the brain, and the hypothalamus, which is a major control center for
homeostasis.
The cerebellum, which is connected to numerous parts of the brain, is critical for
coordinating movement. It is an integration center that decides how to best
execute the desired movement, given the body’s current position and the
muscles’ current status.
The brain stem is composed of the midbrain, the pons, and the medulla
oblongata.
The spinal cord contains both sensory and motor fibers that transmit action
potentials between the brain and the periphery.
Peripheral Nervous System
The PNS contains 43 pairs of nerves: 12 pairs of cranial nerves that
connect with the brain and 31 pairs of spinal nerves that connect
with the spinal cord. Cranial and spinal nerves directly supply the
skeletal muscles. Functionally, the PNS has two major divisions: the
sensory division and the motor division.
Sensory Division
The sensory division of the PNS carries sensory information toward
the CNS. Sensory (afferent) neurons originate in such areas as
blood vessels, internal organs, muscles and tendons, the skin, and
sensory organs (taste, touch, smell, hearing, vision).
Sensory neurons in the PNS end in either the spinal cord or the
brain and continuously convey information to the CNS concerning
the body’s constantly changing status, position, and internal and
external environment. Sensory neurons within the CNS carry the
sensory input to appropriate areas of the brain, where the
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information can be processed and integrated with other incoming
information.
The sensory division receives information from five primary types
of receptors:
1. Mechanoreceptors that respond to mechanical forces such as
pressure, touch, vibrations, or stretch
2. Thermoreceptors that respond to changes in temperature
3. Nociceptors that respond to painful stimuli
4. Photoreceptors that respond to electromagnetic radiation
(light) to allow vision
5. Chemoreceptors that respond to chemical stimuli, such as
from foods, odors, or changes in blood or tissue
concentrations of substances like oxygen, carbon dioxide,
glucose, and electrolytes
Virtually all of these receptors are important in exercise and sport.
Special muscle and joint nerve endings are of many types and
functions, and each type is sensitive to a specific stimulus. Here are
some important examples:
Free nerve endings detect crude touch, pressure, pain, heat,
and cold. Thus, they function as mechanoreceptors,
nociceptors, and thermoreceptors. These nerve endings are
important for preventing injury during athletic performance.
Joint kinesthetic receptors located in the joint capsules are
sensitive to joint angles and rates of change in these angles.
Thus, they sense the position and any movement of the
joints.
Muscle spindles sense muscle length and rate of change in
length.
Golgi tendon organs detect the tension applied by a muscle
to its tendon, providing information about the strength of
muscle contraction.
Muscle spindles and Golgi tendon organs are discussed in more
detail later in this chapter.
Motor Division
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The CNS transmits information to various parts of the body through
the motor, or efferent, division of the PNS. Once the CNS has
processed the information it receives from the sensory division, it
determines how the body should respond to that input. From the
brain and spinal cord, intricate networks of neurons go out to all
parts of the body, providing detailed instructions to the target areas
including—and central to exercise and sport physiology—muscles.
Autonomic Nervous System
The autonomic nervous system, often considered part of the motor
division of the PNS, controls the body’s involuntary internal
functions. Some of these functions that are important to sport and
activity are heart rate, blood pressure, blood distribution, and lung
function.
The autonomic nervous system has two major divisions: the
sympathetic nervous system and the parasympathetic nervous
system. These originate from different sections of the spinal cord
and from the base of the brain. The effects of the two systems are
often antagonistic, but the systems always function together.
Sympathetic Nervous System
The sympathetic nervous system is sometimes called the fight-orflight system: It prepares the body to face a crisis and sustains its
function during the crisis. When fully engaged, the sympathetic
nervous system can produce a massive discharge throughout the
body, preparing it for action. A sudden loud noise, a life-threatening
situation, or those last few seconds before the start of an athletic
competition are examples of circumstances in which this massive
sympathetic excitation may occur. The effects of sympathetic
stimulation are important during exercise. To give a few examples:
Heart rate and strength of cardiac contraction increase.
Coronary vessels dilate, increasing the blood supply to the
heart muscle to meet its increased demands.
Peripheral vasodilation increases blood flow to active skeletal
muscles.
Vasoconstriction in most other tissues diverts blood away
from them and to the active muscles.
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Blood pressure increases, allowing better perfusion of the
muscles and improving the return of venous blood to the
heart.
Bronchodilation improves ventilation and effective gas
exchange.
Metabolic rate increases, reflecting the body’s effort to meet
the increased demands of physical activity.
Mental activity increases, allowing better perception of
sensory stimuli and more concentration on performance.
Glucose is released from the liver into the blood as an energy
source.
Functions not directly needed at that time are slowed (e.g.,
renal function, digestion).
These basic alterations in bodily function facilitate motor responses,
demonstrating the importance of the autonomic nervous system in
preparing the body for and sustaining it during acute stress or
physical activity.
Parasympathetic Nervous System
The parasympathetic nervous system can be thought of as the
body’s housekeeping system. It has a major role in carrying out such
processes as digestion, urination, glandular secretion, and
conservation of energy. This system is more active when one is calm
and at rest. Its effects tend to oppose those of the sympathetic
system. The parasympathetic division causes decreased heart rate,
constriction of coronary vessels, and bronchoconstriction.
The various effects of the sympathetic and parasympathetic
divisions of the autonomic nervous system are summarized in table
3.1.
In Review
The PNS contains 43 pairs of nerves: 12 cranial and 31 spinal.
The PNS can be subdivided into the sensory and motor divisions. The motor
division also includes the autonomic nervous system.
The sensory division carries information from sensory receptors to the CNS. The
motor division carries motor impulses from the CNS to the muscles and other
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organs.
The autonomic nervous system includes the sympathetic nervous system and
the parasympathetic system. Although these systems often oppose each other,
they always function together to create an appropriately balanced response.
Sensory-Motor Integration
Having discussed the components and divisions of the nervous
system, we now discuss how a sensory stimulus gives rise to a
motor response. How, for example, do the muscles in the hand know
to pull one’s finger away from a hot stove? When someone decides
to run, how do the muscles in the legs coordinate while supporting
weight and propelling the person forward? To accomplish these
tasks, the sensory and motor systems must communicate with each
other.
This process is called sensory-motor integration, and it is
depicted in figure 3.7. For the body to respond to sensory stimuli, the
sensory and motor divisions of the nervous system must function
together in the following sequence of events:
1. A sensory stimulus is received by sensory receptors (e.g.,
pinprick).
2. The sensory action potential is transmitted along sensory
neurons to the CNS.
3. The CNS interprets the incoming sensory information and
determines which response is most appropriate, or reflexively
initiates a motor response.
4. The action potentials for the response are transmitted from
the CNS along α-motor neurons.
5. The motor action potential is transmitted to a muscle, and the
response occurs.
TABLE 3.1 Effects of the Sympathetic and Parasympathetic
Nervous Systems on Various Organs
Target organ or system
Sympathetic effects
Parasympathetic
effects
Heart muscle
Increases rate and force of contraction
Heart: coronary blood vessels
Causes vasodilation
Decreases rate of
contraction
Causes
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Lungs
Causes bronchodilation; mildly constricts blood vessels
Blood vessels
Liver
Cellular metabolism
Adipose tissue
Sweat glands
Adrenal glands
Digestive system
Increases blood pressure; causes vasoconstriction in abdominal
viscera and skin to divert blood when necessary; causes vasodilation
in the skeletal muscles and heart during exercise
Stimulates glucose release
Increases metabolic rate
Stimulates lipolysisa
Increases sweating
Stimulates secretion of epinephrine and norepinephrine
Decreases activity of glands and muscles; constricts sphincters
Kidney
Causes vasoconstriction; decreases urine formation
aLipolysis
vasoconstriction
Causes
bronchoconstriction
Has little or no effect
Has no effect
Has no effect
Has no effect
Has no effect
Has no effect
Increases peristalsis
and glandular
secretion; relaxes
sphincters
Has no effect
is the process of breaking down triglyceride into its basic units to be used for energy.
FIGURE 3.7 The sequence of events in sensory-motor integration.
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Sensory Input
Recall that sensations and physiological status are detected by
sensory receptors throughout the body. The action potentials
resulting from sensory stimulation are transmitted via the sensory
nerves to the spinal cord. When they reach the spinal cord, they can
either trigger a local reflex at that level or travel to the upper regions
of the spinal cord or to the brain. Sensory pathways to the brain can
terminate in sensory areas of the brain stem, the cerebellum, the
thalamus, or the cerebral cortex. An area in which the sensory
impulses terminate is referred to as an integration center. This is
where the sensory input is interpreted and linked to the motor
system. Figure 3.8 illustrates various sensory receptors and their
nerve pathways back to the spinal cord and up into various areas of
the brain. The integration centers vary in function:
Sensory impulses that terminate in the spinal cord are
integrated there. The response is typically a simple motor
reflex, which is the simplest type of integration.
Sensory signals that terminate in the lower brain stem result
in subconscious motor reactions of a higher and more
complex nature than simple spinal cord reflexes. Postural
control during sitting, standing, or moving is an example of
this level of sensory input.
Sensory signals that terminate in the cerebellum also result
in subconscious control of movement. The cerebellum
appears to be the center of coordination, smoothing out
movements by coordinating the actions of the various
contracting muscle groups to perform the desired movement.
Both fine and gross motor movements appear to be
coordinated by the cerebellum in concert with the basal
ganglia. Without the control exerted by the cerebellum, all
movement would be uncontrolled and uncoordinated.
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FIGURE 3.8 The sensory receptors and their afferent pathways back to the spinal cord and brain.
Sensory signals that terminate at the thalamus begin to enter
the level of consciousness, and the person begins to
distinguish various sensations.
Only when sensory signals enter the cerebral cortex can one
discretely localize the signal. The primary sensory cortex,
located in the postcentral gyrus (in the parietal lobe),
receives general sensory input from receptors in the skin and
from proprioceptors in the muscles, tendons, and joints. This
area has a map of the body. Stimulation in a specific area of
the body is recognized, and its exact location is known
instantly. Thus, this part of the conscious brain allows us to
be constantly aware of our surroundings and our relationship
to them.
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Once a sensory impulse is received, it may evoke a motor
response, regardless of the level at which the sensory impulse stops.
This response can originate from any of three levels:
The spinal cord
The lower regions of the brain
The motor area of the cerebral cortex
As the level of control moves from the spinal cord to the motor
cortex, the degree of movement complexity increases from simple
reflex control to complicated movements requiring basic thought
processes. Motor responses for more complex movement patterns
typically originate in the motor cortex of the brain, and the basal
ganglia and cerebellum help to coordinate repetitive movements and
to smooth out overall movement patterns. Sensory-motor integration
may also involve reflex pathways for quick responses and
specialized sensory organs within muscles.
Reflex Activity
What happens when one unknowingly puts one’s hand on a hot
stove? First, the stimuli of heat and pain are received by the
thermoreceptors and nociceptors in the hand, and then sensory
action potentials travel to the spinal cord, terminating at the level of
entry. Once in the spinal cord, these action potentials are integrated
instantly by interneurons that connect the sensory and motor
neurons. The action potentials move to the motor neurons and travel
to the effectors, the muscles controlling the withdrawal of the hand.
The result is that the person reflexively withdraws the hand from the
hot stove without giving the action any thought.
A motor reflex is a preprogrammed response; any time the
sensory nerves transmit certain action potentials, the body responds
instantly and identically. In examples like the one just used, whether
one touches something that is too hot or too cold, thermoreceptors
will elicit a reflex to withdraw the hand. Whether the pain arises from
heat or from a sharp object, the nociceptors will also cause a
withdrawal reflex. By the time one is consciously aware of the
specific stimulus (after sensory action potentials also have been
transmitted to the primary sensory cortex), the reflex activity is well
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under way, if not completed. All neural activity occurs extremely
rapidly, but a reflex is the fastest mode of response because the
impulse is not transmitted up the spinal cord to the brain before an
action occurs. Only one response is possible; no options need to be
considered.
RESEARCH PERSPECTIVE 3.3
Sex Differences in Skeletal Muscle Fiber Types
As discussed in this chapter, and in chapter 1, skeletal muscle is made up of
different types of fibers that vary in terms of their structure, biochemistry, and
function. The fiber-type composition of different skeletal muscles depends in
part on the anatomical location and function of the muscle. However,
relatively little is known about whether the proportion of the different fiber
types within a skeletal muscle differs between men and women. To date, the
few studies that have assessed differential fiber-type composition between
sexes have been conducted in rats and mice. In studies that examined sex
differences in humans, the fibers measured in men had significantly larger
cross-sectional areas, which is not surprising because men have an overall
greater muscle mass. However, it appears that women have more type I
fibers and fewer type II fibers than their male counterparts on average. When
fiber-type composition was examined in the vastus lateralis muscle of a group
of men, the average fiber type percentages were 34% type I, 46% type IIa,
and 20% type IIx. In women, the percentages were 41% type I, 36% type IIa,
and 23% type IIx. This greater prevalence of slow-twitch fibers in women
corresponds with a lower contractile velocity in women compared to men but
allows for increased endurance and recovery in women.8 These data
highlight sex differences in muscle fiber-type composition beyond that
associated with muscle size alone. This has important implications. Future
studies examining skeletal muscle composition, function, and adaptive
responses to different forms of exercise training, as well as in
pathophysiological conditions, should consider potential sex differences.
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FIGURE 3.9 (a) A muscle belly showing (b) a muscle spindle and (c) a Golgi tendon organ.
Muscle Spindles
Now that we have covered the basics of reflex activity, we can look
more closely at two specific reflexes that help control muscle
function. The first involves a special structure: the muscle spindle
(see figure 3.9).
The muscle spindle is a group of specialized muscle fibers found
between regular skeletal muscle fibers, referred to as extrafusal
(outside the spindle) fibers. A muscle spindle consists of 4 to 20
small, specialized intrafusal (inside the spindle) fibers and the nerve
endings, sensory and motor, associated with these fibers. A
connective tissue sheath surrounds the muscle spindle and attaches
to the endomysium of the extrafusal fibers. The intrafusal fibers are
controlled by specialized motor neurons, referred to as γ-motor
neurons (or gamma motor neurons). In contrast, extrafusal fibers
(the regular fibers) are controlled by α-motor neurons.
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The central region of an intrafusal fiber cannot contract because it
contains no or only a few actin and myosin filaments. This central
region can only stretch. Because the muscle spindle is attached to
the extrafusal fibers, any time those fibers are stretched, the central
region of the muscle spindle is also stretched.
Sensory nerve endings wrapped around this central region of the
muscle spindle transmit information to the spinal cord when this
region is stretched, transmitting a signal to the CNS about the
muscle’s length. In the spinal cord, the sensory neuron synapses
with an α-motor neuron, which triggers reflexive muscle contraction
(in the extrafusal fibers) to resist further stretching.
Let’s illustrate this action with an example. A person’s arm is bent
at the elbow, and the hand is extended, palm up. Suddenly someone
places a heavy weight in the palm. The forearm starts to drop, which
stretches the muscle fibers in the elbow flexors (e.g., biceps brachii),
which in turn stretch the muscle spindles. In response to that stretch,
the sensory neurons send action potentials to the spinal cord, which
then activates the α-motor neurons of motor units in the same
muscles. This activation causes the muscles to increase their force
production, overcoming the stretch.
γ-Motor neurons excite the intrafusal fibers, prestretching them
slightly. Although the midsection of the intrafusal fibers cannot
contract, the ends can. The γ-motor neurons cause slight contraction
of the ends of these fibers, which stretches the central region slightly.
This prestretch makes the muscle spindle highly sensitive to even
small degrees of stretch.
The muscle spindle also assists normal muscle action. It appears
that when the α-motor neurons are stimulated to contract the
extrafusal muscle fibers, the γ-motor neurons are also activated,
contracting the ends of the intrafusal fibers. This stretches the
central region of the muscle spindle, giving rise to sensory impulses
that travel to the spinal cord and then to the α-motor neurons. In
response, the muscle increases its force production. Thus, muscle
force production is enhanced through this function of the muscle
spindles.
Information brought into the spinal cord from the sensory neurons
associated with muscle spindles does not merely end at that level.
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Impulses are also sent up to higher parts of the CNS, supplying the
brain with continuous feedback on the exact length of the muscle
and the rate at which that length is changing. This information is
essential for maintaining muscle tone and posture and for executing
movements. The muscle spindle functions as a servomechanism to
continuously correct movements that do not proceed as planned.
The brain is informed of errors in the intended movement at the
same time that the error is being corrected at the spinal cord level.
Golgi Tendon Organs
Golgi tendon organs are encapsulated sensory receptors through
which a small bundle of muscle tendon fibers pass. These organs
225
are located just proximal to the tendon fibers’ attachment to the
muscle fibers, as shown in figure 3.9. Approximately 5 to 25 muscle
fibers are usually connected with each Golgi tendon organ. Whereas
muscle spindles monitor the length of a muscle, Golgi tendon organs
are sensitive to tension in the muscle–tendon complex and operate
like a strain gauge, a device that senses changes in tension. Their
sensitivity is so great that they can respond to the contraction of a
single muscle fiber. These sensory receptors are inhibitory in nature,
performing a protective function by reducing the potential for injury.
When stimulated, these receptors inhibit the contracting (agonist)
muscles and excite the antagonist muscles.
In Review
Sensory-motor integration is the process by which the PNS relays sensory input
to the CNS and the CNS interprets this information and then sends out the
appropriate motor signal to elicit the desired motor response.
The level of nervous system response to sensory input varies according to the
complexity of movement necessary. Most simple reflexes are handled by the
spinal cord, whereas complex reactions and movements require activation of
higher centers in the brain.
Sensory input can terminate at various levels of the CNS. Not all of this
information reaches the brain.
Reflexes are the simplest form of motor control. These are not conscious
responses. For a given sensory stimulus, the motor response is always identical
and instantaneous.
Muscle spindles trigger reflexive muscle action when stretched.
Golgi tendon organs trigger a reflex that inhibits contraction if the tendon fibers
are stretched from high muscle tension.
RESEARCH PERSPECTIVE 3.4
Nontraditional Factors That Impair Neuromuscular
Control
Lower-extremity musculoskeletal injuries that occur during sport and physical
activity, such as anterior cruciate ligament (ACL) tears, are far too common
and extremely costly. Furthermore, these injuries are associated with serious
long-term consequences beyond the injury itself, including the accelerated
226
development of osteoarthritis. The first step toward effectively preventing
lower-extremity injuries is the appropriate identification of the important risk
factors for injury.
Perhaps the most commonly considered primary injury risk factors are
measures of neuromuscular control, such as balance and movement
technique. However, beyond these traditional risk factors, it is important to
consider nontraditional factors that may predispose the athlete to injury, such
as alterations in hydration, increases in body temperature, and fatigue.
Importantly, hypohydration (below-optimal body fluid balance), hyperthermia
(increased body core temperature), and fatigue, which are likely to be
encountered during physical activity, all impair neuromuscular control. A 2012
study has substantiated this finding.3 In particular, hypohydration combined
with hyperthermia negatively affected movement technique and, to a lesser
extent, balance. These findings emphasize the need for adequate hydration
during exercise, especially when performed in hot environments, not only to
optimize performance and prevent heat-related complications (see chapter
12), but also to reduce the risk of lower-extremity injury.1
Golgi tendon organs are important in resistance exercise. They
function as safety devices, helping to prevent the muscle from
developing excessive force during a contraction that may ultimately
damage the muscle. Additionally, some researchers speculate that
reducing the influence of Golgi tendon organs disinhibits the active
muscles, allowing a more forceful muscle action. This mechanism
may explain at least part of the gains in muscular strength that
accompany strength training.
Motor Response
Now that we have discussed how sensory input is integrated to
determine the appropriate motor response, the last step in the
process is how muscles respond to motor action potentials once they
reach the muscle fibers.
Once an action potential reaches an α-motor neuron, it travels the
length of the neuron to the NMJ. From there, the action potential
spreads to all muscle fibers innervated by that particular α-motor
neuron. Recall that the α-motor neuron and all muscle fibers it
innervates form a single motor unit. Each muscle fiber is innervated
by only one α-motor neuron, but each α-motor neuron innervates up
to several thousand muscle fibers, depending on the function of the
muscle. Muscles controlling fine movements have only a small
227
number of muscle fibers per α-motor neuron. The muscles that
control eye movements (the extraocular muscles) have an
innervation ratio of 1:15, meaning that one α-motor neuron controls
only 15 muscle fibers. Muscles with more general functions have
many fibers per α-motor neuron. For example, the gastrocnemius
and tibialis anterior muscles of the lower leg have innervation ratios
of almost 1:2,000.
The muscle fibers in a specific motor unit are homogeneous with
respect to fiber type. Thus, one will not find a motor unit that has
both type II and type I fibers. In fact, as mentioned in chapter 1, it is
generally believed that the characteristics of the α-motor neuron
actually determine the fiber type in the given motor unit.7
228
IN CLOSING
In this chapter, we examined how the nervous system is organized and how
that organization functions to control movement. We covered the central
nervous system as it relates to movement and the sensory and effector arms of
the peripheral nervous system. We have seen how muscles respond to neural
stimulation, whether through reflexes or under complex control of the higher
brain centers, and the role of individual motor units in determining this
response. Thus, we have learned how the body functions to allow people to
move. In the next chapter, we examine the role of hormones in the body’s
response to exercise.
KEY TERMS
acetylcholine
adrenergic
axon hillock
axon terminal
central nervous system (CNS)
cholinergic
depolarization
effector (efferent) nerves
end branches
excitatory postsynaptic potential (EPSP)
Golgi tendon organ
graded potential
hyperpolarization
inhibitory postsynaptic potential (IPSP)
motor neurons (motor nerves)
motor reflex
muscle spindle
myelin sheath
nerve impulse
neuromuscular junction
neuron
neurotransmitter
norepinephrine
peripheral nervous system (PNS)
resting membrane potential (RMP)
saltatory conduction
sensory (afferent) nerves
229
sensory-motor integration
sodium–potassium pump
synapse
threshold
STUDY QUESTIONS
1.
What are the major divisions of the nervous system? What are their major
functions?
2.
Name the different anatomical parts of a neuron, and discuss their
function.
3.
Explain the resting membrane potential. What causes it? How is it
maintained?
4.
Describe an action potential. What is required before an action potential is
activated?
5.
Explain how an action potential is transmitted from a presynaptic neuron to
a postsynaptic neuron. Describe a synapse and a neuromuscular junction.
6.
What brain centers have major roles in controlling movement, and what
are these roles?
7.
How do the sympathetic and parasympathetic systems differ? What is their
significance in performing physical activity?
8.
9.
10.
Explain how reflex movement occurs in response to touching a hot object.
Describe the role of the muscle spindle in controlling muscle contraction.
Describe the role of the Golgi tendon organ in controlling muscle
contraction.
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter
QUIZ tests your understanding of the material covered in the chapter.
230
231
4
Hormonal Control During Exercise
In this chapter and in the web study guide
The Endocrine System
Chemical Classification of Hormones
Hormone Secretion and Plasma Concentration
Hormone Actions
ACTIVITY 4.1 Endocrine Glands reviews the body’s major endocrine glands.
ANIMATION FOR FIGURE 4.2 shows the mechanism of action of a steroid hormone.
ANIMATION FOR FIGURE 4.3 shows the mechanism of action of a nonsteroid hormone.
Endocrine Glands and Their Hormones: An Overview
ACTIVITY 4.2 Hormones reviews hormones and their functions.
VIDEO 4.1 presents Katarina Borer on the contributing role of sex hormones to ACL tears in women.
Hormonal Regulation of Metabolism During Exercise
Endocrine Glands Involved in Metabolic Regulation
Regulation of Carbohydrate Metabolism During Exercise
Regulation of Fat Metabolism During Exercise
AUDIO FOR FIGURE 4.4 describes changes in key hormones and blood glucose during prolonged
exercise.
AUDIO FOR FIGURE 4.5 describes changes in blood glucose and insulin levels during prolonged
exercise.
Hormonal Regulation of Fluid and Electrolytes During Exercise
Endocrine Glands Involved in Fluid and Electrolyte Homeostasis
The Kidneys as Endocrine Organs
ANIMATION FOR FIGURE 4.7 describes the role of ADH in conserving body fluid during exercise.
ANIMATION FOR FIGURE 4.8 explores the renin-angiotensin-aldosterone mechanism.
AUDIO FOR FIGURE 4.9 describes changes in plasma volume and aldosterone concentration during
exercise.
232
ACTIVITY 4.3 Hormones and Exercise considers hormones and their key roles in maintaining
homeostasis during physical activity.
Hormonal Regulation of Caloric Intake
Gastrointestinal Tract Hormones
Adipose Tissue as an Endocrine Organ
Effects of Acute and Chronic Exercise on Satiety Hormones
ANIMATION FOR FIGURE 4.10 describes the regulation of appetite by the hormones ghrelin and leptin.
In Closing
233
O
n May 22, 2010, a 13-year-old American boy became the youngest climber
to reach the top of Mount Everest, a grueling trek to an altitude 29,035 ft (8,850 m)
above sea level. The climb was extremely controversial because of the boy’s age. In
fact, because the Nepalese government would not give the family permission to
climb Everest from Nepal, the climbing team ascended from the more difficult
Chinese side where there was no age restriction. To prepare for the climb, the boy
and his father (and climbing partner) slept for months in a hypoxic tent to prepare
their bodies for ascent to high altitude. One goal of high-altitude acclimation is to
increase the concentration of oxygen-carrying red blood cells in the blood. Two
important hormones facilitated this goal. An increase in the hormone erythropoietin
signaled the bone marrow to produce more red blood cells, and a decrease in
vasopressin (also called antidiuretic hormone) caused the kidneys to produce
excess urine to better concentrate the red blood cells. Because of these
adaptations, the climbers were able to summit Mount Everest with less time spent in
the various base camps along the way.
During exercise and exposure to extreme environments, the body
must make a multitude of physiological adjustments. Energy
production must increase, and metabolic by-products must be
cleared. Cardiovascular and respiratory function must be constantly
adjusted to match the demands placed upon these and other body
systems, such as those regulating temperature. While the body’s
internal environment is in a constant state of flux even at rest, during
exercise these well-orchestrated changes must occur rapidly and in a
well-coordinated manner.
While much of the physiological regulation and integration required
during exercise is accomplished by the nervous system (discussed in
chapter 3), another physiological system—the endocrine system—
affects virtually every cell, tissue, and organ in the body. It constantly
monitors the body’s internal environment, noting all changes that
occur and rapidly releasing hormones to ensure that homeostasis is
not dramatically disrupted. In this chapter, we focus on the
importance of hormones in maintaining homeostasis and aiding all
the internal processes that support physical activity. Because we
cannot cover all aspects of endocrine control during exercise, the
focus is on hormonal control of metabolism and body fluid balance
234
during exercise. Because diet plays an important role in exercise
metabolism, hormonal regulation of food intake is also covered.
Additional hormones—including those that regulate growth and
development, muscle mass, and reproductive function—are covered
in other chapters of this book.
The Endocrine System
As the body transitions from a resting to an active state, the rate of
metabolism must increase to provide necessary energy. This requires
the coordinated integration and communication of many physiological
and biochemical systems. Although the nervous system is
responsible for much of this communication, fine-tuning the
physiological responses to any disturbance in homeostasis is
primarily the responsibility of the endocrine system. The endocrine
and nervous systems, often collectively called the neuroendocrine
system, work in concert to control all of the physiological processes
that support exercise. The nervous system functions quickly, having
short-lived, localized effects, whereas the endocrine system responds
more slowly but has longer-lasting effects.
The endocrine system is defined as all tissues or glands that
secrete hormones. The major endocrine glands and tissues are
illustrated in figure 4.1. Endocrine glands typically secrete their
hormones directly into the blood where they act as chemical signals
throughout the body. When secreted by the specialized endocrine
cells, hormones are transported via the blood to specific target cells
—cells that possess specific hormone receptors. On reaching their
destinations, hormones can control the activity of the target tissue.
Historically, hormones were defined as chemicals made by a gland
that traveled to a remote tissue in the body to exert their action. Now
hormones are more broadly defined as any chemical that controls
and regulates the activity of certain cells or organs. Some hormones
affect many body tissues, including the brain, whereas others target
specific cells within a tissue.
Hormones are involved in most physiological processes, so their
actions are relevant to many aspects of exercise and physical activity.
Because hormones play key roles in almost every system of the body,
total coverage of that topic is well beyond the scope of this book. In
235
the following sections, the chemical nature of hormones and the
general mechanisms through which they act are discussed. An
overview of the major endocrine glands and their hormones is
presented for completeness. With respect to exercise, the focus is on
two major aspects of hormonal control, the control of exercise
metabolism and the regulation of body fluids and electrolytes during
exercise. Finally, new information about hormonal regulation of food
intake is presented, since caloric intake and specific nutrients
consumed have a profound influence on exercise metabolism.
Chemical Classification of Hormones
Hormones are traditionally categorized as steroid hormones and
nonsteroid hormones. Steroid hormones have a chemical structure
similar to cholesterol, since most are derived from cholesterol. For
this reason, they are soluble in lipids so they diffuse rather easily
through cell membranes. This group includes the reproductive
hormones testosterone (secreted by the testes) and estrogen and
progesterone (secreted by the ovaries and placenta), as well as
cortisol and aldosterone (secreted by the adrenal cortex).
236
FIGURE 4.1 Location of the major endocrine organs of the body.
Nonsteroid hormones are not lipid soluble, so they cannot easily
cross cell membranes. The nonsteroid hormone group can be
subdivided into two groups: protein or peptide hormones and amino
acid–derived hormones. The two hormones produced by the thyroid
gland (thyroxine and triiodothyronine) and the two from the adrenal
medulla (epinephrine and norepinephrine) are amino acid–derived
hormones. All other nonsteroid hormones are protein or peptide
hormones. The chemical structure of a hormone determines its
mechanism of action on target cells and tissues.
Hormone Secretion and Plasma Concentration
237
Control of hormone secretion must be rapid in order to meet the
demands of changing bodily functions. Hormones are not secreted
constantly or uniformly, but often in a pulsatile manner, that is, in
irregularly timed brief bursts. Therefore, plasma concentrations of
specific hormones fluctuate over short periods of an hour or less. But
plasma concentrations of many hormones also fluctuate over longer
periods of time, showing daily or even monthly cycles (such as
monthly menstrual cycles). How do endocrine glands know when to
release their hormones and how much to release?
Negative feedback is the primary mechanism through which the
endocrine system maintains homeostasis. Secretion of a hormone
causes some change in the body, and this change in turn inhibits
further hormone secretion. Consider how a home thermostat works.
When the room temperature decreases below some preset level, the
thermostat signals the furnace to produce heat. When the room
temperature increases to the preset level, the thermostat’s signal
ends, and the furnace stops producing heat. In the body, secretion of
a specific hormone is similarly turned on or off (or up or down) by
specific physiological changes.
Using the example of plasma glucose concentrations and the
hormone insulin, when the plasma glucose concentration is high, the
pancreas releases insulin. Insulin increases cellular uptake of
glucose, lowering plasma glucose concentration. When plasma
glucose concentration returns to normal, insulin release is inhibited
until the plasma glucose level increases again. Because the
endocrine system works in concert with the nervous system, the
central nervous system is also involved in maintenance of appropriate
hormonal balance.
The plasma concentration of a specific hormone is not always the
best indicator of that hormone’s activity because hormones must bind
to specific cellular receptors to exert an effect. Accordingly, the
number of receptors on target cells can be altered to increase or
decrease that cell’s sensitivity to the hormone. With fewer receptors,
fewer hormone molecules can bind, and the cell becomes less
sensitive to the given hormone. This is referred to as
downregulation, or desensitization. In people with insulin
resistance, for example, the number of insulin receptors on their
238
cells appears to be reduced. Their bodies respond by increasing
insulin secretion from the pancreas, so their plasma insulin
concentrations increase. To obtain the same degree of plasma
glucose control as normal, healthy people, these individuals must
release much more insulin.
In a few instances, a cell may respond to the prolonged presence
of large amounts of a hormone by increasing its number of available
receptors. When this happens, the cell becomes more sensitive to
that hormone because more can be bound at one time. This is
referred to as upregulation. For example, individuals with a high
insulin sensitivity, the opposite of insulin resistance, need relatively
normal or low levels of insulin to process a given concentration of
blood glucose.
Hormone Actions
Because hormones travel in the blood, they contact virtually all body
tissues. How, then, do they limit their effects to specific targets? This
ability is attributable to the specific hormone receptors on target
tissues that can bind only specific hormones. Each cell typically has
from 2,000 to 10,000 receptors. The combination of a hormone and
its bound receptor is referred to as a hormone–receptor complex.
Recall that steroid hormones are lipid soluble and can therefore
pass through cell membranes whereas nonsteroid hormones cannot.
Receptors for nonsteroid hormones are located on the cell
membrane, while those for steroid hormones are found either in the
cytoplasm or in the nucleus of the cell. Each hormone is usually
highly specific for a single type of receptor and binds only with its
specific receptors, thus affecting only tissues that contain those
specific receptors. Once hormones are bound to a receptor,
numerous mechanisms allow them to control the actions of those
cells.
Steroid Hormones
The general mechanism of action of steroid hormones is illustrated in
figure 4.2. Once through the cell membrane and inside the cell, a
steroid hormone binds to its specific receptors. The hormone–
receptor complex then enters the nucleus, binds to part of the cell’s
DNA (deoxyribonucleic acid), and activates certain genes. This
239
process is referred to as direct gene activation. In response to this
activation, mRNA (messenger ribonucleic acid) is synthesized within
the nucleus. The mRNA then enters the cytoplasm and promotes
protein synthesis. These proteins may be
enzymes that can have numerous effects on cellular
processes,
structural proteins for tissue growth and repair, or
regulatory proteins that can alter enzyme function.
FIGURE 4.2 The general mechanism of action of a typical steroid hormone, leading to direct gene
activation and protein synthesis.
Nonsteroid Hormones
240
Because nonsteroid hormones cannot cross the cell membrane, they
bind with specific receptors on the cell membrane. A nonsteroid
hormone molecule binds to its membrane receptor and triggers a
series of reactions that lead to the formation of an intracellular
second messenger. In addition to relaying signals, second
messengers can also help intensify the strength of the signal. While
there are many second messenger molecules, one important second
messenger that mediates multiple hormone–receptor responses is
cyclic adenosine monophosphate (cAMP, or cyclic AMP); its
mechanism of action is depicted in figure 4.3. In this case, attachment
of the hormone to the appropriate membrane receptor activates an
enzyme, adenylate cyclase, situated within the cell membrane. This
enzyme regulates the formation of cAMP from cellular adenosine
triphosphate (ATP). Cyclic AMP then controls specific physiological
responses that can include
activation of cellular enzymes,
change in membrane permeability,
promotion of protein synthesis,
change in cellular metabolism, or
stimulation of cellular secretions.
Some of the hormones that employ cAMP as a second messenger
are epinephrine, glucagon, and luteinizing hormone. In addition to
cAMP, other important second messengers include cyclic guanosine
monophosphate (cGMP), inositol trisphosphate (IP3), diacylglycerol
(DAG), and calcium ions (Ca2+).
Although by strict definition not hormones, prostaglandins are
often considered to be a third class of hormones. These substances
are derived from a fatty acid, arachidonic acid, and they are
associated with the plasma membranes of almost all body cells.
Prostaglandins typically act as local hormones or autocrines,
exerting their effects in the immediate area where they are produced.
But some also survive long enough to circulate through the blood to
affect distant tissues. Prostaglandin release can be triggered by many
stimuli, such as other hormones or a local injury. Their functions are
quite numerous because there are several different types of
prostaglandins. They often mediate the effects of other hormones.
241
They are also known to act directly on blood vessels, increasing
vascular permeability (which promotes swelling) and vasodilation. In
this capacity, they are important mediators of the inflammatory
response. They also sensitize the nerve endings of pain fibers; thus,
they mediate both inflammation and pain.
FIGURE 4.3 The mechanism of action of a nonsteroid hormone, in this case activating a second
messenger (cyclic adenosine monophosphate) within the cell to activate cellular functions.
Endocrine Glands and Their Hormones: An
Overview
The major endocrine glands and their respective hormones are listed
in table 4.1. This table also lists each hormone’s primary target and
actions. Because the endocrine system is extremely complex, the
242
presentation here has been greatly simplified to focus on those
endocrine glands and hormones of greatest importance to exercise
and physical activity.
Because hormones play such an important role in regulation of
many physiological variables during exercise, it is not surprising that
hormone release changes during acute bouts of activity. The
hormonal responses to an acute bout of exercise and to exercise
training are summarized in table 4.2. This table is limited to those
hormones that play major roles in sport and physical activity. Further
details of these exercise-induced hormonal responses are provided in
the following discussion of specific endocrine glands and their
hormones.
243
244
TABLE 4.2 Hormone Responses to Acute Exercise and
Change in Response With Exercise Training
245
Endocrine
gland
Hormone
Response to acute exercise (untrained)
Effect of exercise training
Anterior
pituitary
Growth hormone (GH)
Increases with increasing rates of work
Thyrotropin (TSH)
Adrenocorticotropin
(ACTH)
Prolactin
Follicle-stimulating
hormone (FSH)
Luteinizing hormone (LH)
Antidiuretic hormone (ADH
or vasopressin)
Oxytocin
Thyroxine (T4) and
triiodothyronine (T3)
Calcitonin
Parathyroid hormone (PTH
or parathormone)
Epinephrine
Increases with increasing rates of work
Increases with increasing rates of work and
duration
Increases with exercise
Small or no change
Attenuated response at same rate of
work
No known effect
Attenuated response at same rate of
work
No known effect
No known effect
Posterior
pituitary
Thyroid
Parathyroid
Adrenal
medulla
Adrenal
cortex
Pancreas
Kidney
Testes
Ovaries
Small or no change
Increases with increasing rates of work
Unknown
Free T3 and T4 increase with increasing rates
of work
Unknown
Increases with prolonged exercise
Increases with increasing rates of work,
Norepinephrine
starting at about 75% of
O2max
Increases with increasing rates of work,
Aldosterone
Cortisol
Insulin
starting at about 50% of
O2max
Increases with increasing rates of work
Increases only at high rates of work
Decreases with increasing rates of work
Glucagon
Increases with increasing rates of work
Renin
Erythropoietin (EPO)
Testosterone
Increases with increasing rates of work
Unknown
Small increases with exercise
Estrogens and
progesterone
Small increases with exercise
No known effect
Attenuated response at same rate of
work
Unknown
Increased turnover of T3 and T4 at
same rate of work
Unknown
Unknown
Attenuated response at same rate of
work
Attenuated response at same rate of
work
Unchanged
Slightly higher values
Attenuated response at same rate of
work
Attenuated response at same rate of
work
Unchanged
Unchanged
Resting levels decreased in male
runners
Resting levels might be decreased in
highly trained women
As mentioned earlier, a comprehensive description of
neuroendocrine control is well beyond the scope of this textbook. Two
important exercise-related functions of the endocrine glands and their
hormones are the regulation of metabolism during exercise and the
regulation of body fluids and electrolytes. The endocrine system also
plays an important role in regulating appetite and food intake. The
sections that follow detail these three important functions. Each
section provides a description of the primary endocrine glands
involved, the hormones produced, and how those hormones serve
the given regulatory role.
VIDEO 4.1 Presents Katarina Borer on the contributing role of sex
hormones to ACL tears in women.
246
In Review
The nervous system functions quickly, having short-lived, localized effects,
whereas the endocrine system typically responds more slowly but has longerlasting effects.
Hormones are classified chemically as either steroid or nonsteroid. Steroid
hormones are lipid soluble, and most are formed from cholesterol. Nonsteroid
hormones are formed from proteins, peptides, or amino acids.
Hormones influence specific target tissues or cells through a unique interaction
between the hormone and the specific receptors for that hormone on the cell
membrane (nonsteroid hormones) or within the cytoplasm or nucleus of the cell
(steroid hormones).
Hormones generally are secreted nonuniformly, often in brief pulsatile bursts, into
the blood and then circulate to target cells.
A negative feedback system regulates secretion of most hormones.
The number of receptors for a specific hormone can be altered to meet the body’s
demands. Upregulation refers to an increase in available receptors, and
downregulation refers to a decrease. These two processes change a cell’s
sensitivity to a given hormone.
Steroid hormones pass through cell membranes and bind to receptors in the
cytoplasm or nucleus of the cell. At the nucleus, they use a mechanism called
direct gene activation to cause protein synthesis.
Nonsteroid hormones cannot easily enter cells, so they bind to receptors on the
cell membrane. This activates a second messenger within the cell, often cAMP,
which in turn can trigger numerous cellular processes.
Prostaglandins are not hormones by strict definition but act as local hormones,
exerting their effect in the immediate area where they are produced.
247
Hormonal Regulation of Metabolism During
Exercise
As noted in chapter 2, carbohydrate and fat metabolism are
responsible for maintaining muscle ATP during prolonged exercise.
Various hormones work to ensure adequate glucose and free fatty
acid (FFA) availability for muscle energy metabolism. In the next
sections, we examine (1) the major endocrine glands and hormones
responsible for metabolic regulation and (2) how the metabolism of
glucose and fat is regulated by these hormones during exercise.
Endocrine Glands Involved in Metabolic Regulation
While many complex systems interact to regulate metabolism at rest
and during exercise, the major endocrine glands responsible are the
anterior pituitary gland, the thyroid gland, the adrenal glands, and the
pancreas.
Anterior Pituitary
The pituitary gland is a marble-sized gland attached to the
hypothalamus at the base of the brain. It has three lobes: anterior,
intermediate, and posterior. The intermediate lobe is very small and is
thought to play little or no role in humans, but both the anterior and
posterior lobes serve major endocrine functions. Hormonal release
from the anterior pituitary is controlled by hormones secreted by the
hypothalamus, while the posterior pituitary releases hormones in
response to direct nerve signals from the hypothalamus. Therefore,
the pituitary gland can be thought of as the relay between CNS
control centers and peripheral endocrine glands. The posterior
pituitary is discussed later in the chapter.
The anterior pituitary, also called the adenohypophysis, secretes
six hormones in response to releasing factors or inhibiting factors
(which are also categorized as hormones) secreted by the
hypothalamus. Hormonal communication between the hypothalamus
and the anterior lobe of the pituitary occurs through a specialized
circulatory system. The major functions of each of the anterior
pituitary hormones, along with their releasing and inhibiting factors,
are listed in table 4.1. Exercise is a strong stimulus to the
248
hypothalamus because exercise increases the release of most
anterior pituitary hormones (see table 4.2).
Of the six anterior pituitary hormones, four are tropic hormones,
meaning they affect the functioning of other endocrine glands. The
exceptions are growth hormone and prolactin. Growth hormone
(GH) is a potent anabolic agent (a substance that builds up organs
and tissues, producing growth and cell differentiation and an increase
in size of tissues). It promotes muscle growth and hypertrophy by
facilitating amino acid transport into the cells. In addition, GH directly
stimulates fat metabolism (lipolysis) by increasing the synthesis of
lipolytic enzymes. Growth hormone concentrations are elevated
during both aerobic and resistance exercise in proportion to the
exercise intensity and typically remain elevated for some time after
exercise.
RESEARCH PERSPECTIVE 4.1
Does Having More Testosterone Give You a Competitive
Advantage?
Androgens (testosterone and its chemical derivatives) stimulate the
development and maintenance of primary and secondary male sex
characteristics. Although androgens are typically described as male sex
hormones, they are found naturally in both men and women and can improve
sport performance in both male and female athletes, particularly in strengthdependent events. Because of their ergogenic effects (enhanced physical
performance, stamina, and recovery), androgens have been widely abused by
athletes despite advances in tests to detect their abuse. In fact, androgens are
the most common ergogenic aid used by female athletes. However, some
women have naturally higher circulating androgens, and a great deal of
controversy has surrounded the debate about whether these women should
be allowed to compete with this natural ergogenic advantage. Because of this
controversy, regulatory committees are keenly interested in scientific evidence
that may link circulating natural androgens and athletic performance.
A recent study of 2,127 elite track and field athletes competing in the 2011
and 2013 International Association of Athletics Federations World
Championships provided more scientific data on this controversial topic.1
Researchers measured blood androgens, particularly testosterone
concentrations, in male and female athletes and compared these
concentrations to each athlete’s best performances at the World
Championships. Male sprinters showed higher testosterone concentrations,
and men involved in throwing events had lower testosterone concentrations
249
than male athletes in other events. The type of event had no association with
testosterone concentration in women. However, women (but not men) with the
highest testosterone concentrations performed better in the 400 m, 400 m
hurdles, 800 m, hammer throw, and pole vault when compared to women with
the lowest testosterone. The study concluded that female athletes with high
natural testosterone concentrations may have a competitive advantage over
those with low testosterone competing in these specific track-and-field events.
Thus, the quantitative relation between elevated testosterone and improved
athletic performance should be considered when regulatory and governing
bodies discuss the eligibility of women with hyperandrogenism in competitive
events.
Thyroid Gland
The thyroid gland is located along the midline of the neck,
immediately below the larynx. It secretes two important nonsteroid
hormones, triiodothyronine (T3) and thyroxine (T4), which regulate
metabolism in general, and an additional hormone, calcitonin, which
assists in regulating calcium metabolism.
The two metabolic thyroid hormones share similar functions.
Triiodothyronine and thyroxine increase the metabolic rate of almost
all tissues and can increase the body’s basal metabolic rate by as
much as 100%. These hormones also
increase protein synthesis (including enzymes),
increase the size and number of mitochondria in most cells,
promote rapid cellular uptake of glucose,
enhance glycolysis and gluconeogenesis, and
enhance lipid mobilization, increasing FFA availability for
oxidation.
Acute exercise causes the release of thyrotropin (TSH, or thyroidstimulating hormone) from the anterior pituitary. Thyroid-stimulating
hormone controls the release of triiodothyronine and thyroxine, so the
exercise-induced increase in TSH would be expected to stimulate the
thyroid gland. Exercise increases plasma thyroxine concentrations,
but a delay occurs between the increase in TSH concentrations
during exercise and the increase in plasma thyroxine concentration.
Furthermore, during prolonged submaximal exercise, thyroxine
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concentration increases sharply, then remains relatively constant
while triiodothyronine concentrations tend to decrease over time.
Adrenal Glands
The adrenal glands are situated directly atop each kidney and are
composed of the inner adrenal medulla and the outer adrenal cortex.
The hormones secreted by these two areas are quite distinct. The
adrenal medulla produces and releases two hormones, epinephrine
and norepinephrine, which are collectively referred to as
catecholamines. Because of its origin in the adrenal gland, a
synonym for epinephrine is adrenaline. When the adrenal medulla is
stimulated by the sympathetic nervous system, approximately 80% of
its secretion is epinephrine and 20% is norepinephrine, although
these percentages vary with different physiological conditions.
Circulating catecholamines have powerful effects similar to those of
the sympathetic nervous system. Recall that these same
catecholamines function as neurotransmitters in the sympathetic
nervous system; however, the hormones’ effects last longer because
these substances are removed from the blood relatively slowly
compared to the quick reuptake and degradation of the
neurotransmitters. These two hormones prepare a person for
immediate action, often called the fight-or-flight response.
Although some of the specific actions of these two hormones differ,
the two work together. Their combined effects include
increased heart rate and force of contraction,
increased metabolic rate,
increased glycogenolysis (breakdown of glycogen to glucose)
in the liver and muscle,
increased release of glucose and FFAs into the blood,
redistribution of blood to the skeletal muscles,
increased blood pressure, and
increased respiration.
Release of epinephrine and norepinephrine is affected by a wide
variety of factors, including psychological stress and exercise.
Plasma concentrations of these hormones increase as individuals
increase
their
exercise
intensity.
Plasma
norepinephrine
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concentrations increase markedly at intensities above 50% of O2max,
but epinephrine concentrations do not increase significantly until the
exercise intensity exceeds 60% to 70% of O2max. During longduration steady-state exercise at a moderate intensity, blood
concentrations of both hormones increase. When the exercise bout
ends, epinephrine returns to resting concentrations within only a few
minutes of recovery, but norepinephrine can remain elevated for
several hours.
The adrenal cortex secretes more than 30 different steroid
hormones, referred to as corticosteroids. These generally are
classified into three major types: mineralocorticoids (discussed later
in the chapter), glucocorticoids, and gonadocorticoids (sex
hormones).
The glucocorticoids are essential to the ability to adapt to
exercise and other forms of stress. They also help maintain fairly
consistent plasma glucose concentrations even during long periods
without ingestion of food. Cortisol, also known as hydrocortisone, is
the major corticosteroid. It is responsible for about 95% of all
glucocorticoid activity in the body. Cortisol
stimulates gluconeogenesis to ensure an adequate fuel
supply;
increases mobilization of FFAs, making them more available
as an energy source;
decreases glucose utilization, sparing it for the brain;
stimulates protein catabolism to release amino acids for use
in repair, enzyme synthesis, and energy production;
acts as an anti-inflammatory agent;
depresses immune reactions; and
increases the vasoconstriction caused by epinephrine.
We discuss cortisol’s important role in exercise later in this chapter
when we consider the regulation of glucose and fat metabolism.
Pancreas
The pancreas is located behind and slightly below the stomach. Its
two major hormones are insulin and glucagon. The balance of these
two opposing hormones provides the major control of plasma glucose
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concentration. When plasma glucose is elevated (hyperglycemia),
as occurs after a meal, the pancreas releases insulin into the blood.
Among its actions, insulin
facilitates glucose transport into the cells, especially muscle
fibers;
promotes glycogenesis; and
inhibits gluconeogenesis.
Insulin’s main function is to reduce the amount of glucose circulating
in the blood. But it is also involved in protein and fat metabolism,
promoting cellular uptake of amino acids and enhancing synthesis of
protein and fat.
The pancreas secretes glucagon when the plasma glucose
concentration falls below normal concentrations (hypoglycemia).
The effects of glucagon generally oppose those of insulin. Glucagon
promotes increased breakdown of liver glycogen to glucose
(glycogenolysis) and increased gluconeogenesis, both of which
increase plasma glucose levels.
During exercise lasting 30 min or longer, the body attempts to
maintain plasma glucose concentrations; however, insulin
concentrations tend to decline. The ability of insulin to bind to its
receptors on muscle cells increases during exercise, due in large part
to increased blood flow to muscle. This increases the body’s
sensitivity to insulin and reduces the need to maintain high plasma
insulin concentrations for transporting glucose into the muscle cells.
Plasma glucagon, on the other hand, shows a gradual increase
throughout exercise. Glucagon primarily maintains plasma glucose
concentrations by stimulating liver glycogenolysis. This increases
glucose availability to the cells, maintaining adequate plasma glucose
concentrations to meet increased metabolic demands. The responses
of these hormones are usually blunted in trained individuals, and
those who are well trained are better able to maintain plasma glucose
concentrations.
Regulation of Carbohydrate Metabolism During Exercise
As we learned in chapter 2, the heightened energy demands of
exercise require that more glucose be made available to the muscles.
Because glucose is stored in the body as glycogen, primarily in the
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muscles and the liver, glycogenolysis must increase to free the
glucose from this storage form. Glucose freed from the liver enters
the blood to circulate throughout the body, allowing it access to active
tissues. Plasma glucose concentration also can be increased through
gluconeogenesis, the production of new glucose from
noncarbohydrate sources like lactate, amino acids, and glycerol.
Regulation of Plasma Glucose Concentration
The plasma glucose concentration during exercise depends on a
balance between glucose uptake by exercising muscles and its
release by the liver. Four hormones work to increase the circulating
plasma glucose:
Glucagon
Epinephrine
Norepinephrine
Cortisol
At rest, glucose release from the liver is facilitated by glucagon,
which promotes both liver glycogen breakdown and glucose
formation from amino acids. During exercise, glucagon secretion
increases, as does the rate of catecholamine release from the
adrenal medulla; these three hormones (glucagon, epinephrine, and
norepinephrine) work in concert to further increase glycogenolysis.
After a slight initial drop, cortisol concentration increases during the
first 30 to 45 min of exercise. Cortisol increases protein catabolism,
freeing amino acids to be used within the liver for gluconeogenesis.
Thus, all four of these hormones can increase plasma glucose by
enhancing the processes of glycogenolysis (breakdown of glycogen)
and gluconeogenesis (making glucose from other substrates). In
addition to the effects of the four major glucose-controlling hormones,
GH increases mobilization of FFAs and decreases cellular uptake of
glucose, so less glucose is used by the cells and more remains in
circulation. The thyroid hormones promote glucose catabolism and fat
metabolism.
The amount of glucose released by the liver depends on both
exercise intensity and duration. As intensity increases, so does the
rate of catecholamine release. This can cause the liver to release
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more glucose than is being taken up by the active muscles.
Consequently, during or shortly after an explosive, short-term sprint,
blood glucose concentrations may be 40% to 50% above the resting
value, since glucose is released by the liver at a greater rate than the
rate of uptake by the muscles.
The greater the exercise intensity, the greater the catecholamine
release, and thus the rate of glycogenolysis is significantly increased.
This process occurs not only in the liver but also in the muscle.
Glucose released from the liver enters the blood, where it becomes
available to the muscle fibers. But the muscle has a more readily
available source of glucose: its own glycogen stores. The muscle
uses its own glycogen stores before using the plasma glucose during
explosive, short-term exercise. Glucose released from the liver is not
used as readily, so it remains in the circulation, elevating the plasma
glucose. Following exercise, plasma glucose concentration
decreases as the glucose enters the muscle to replenish the depleted
muscle glycogen stores (glycogenolysis).
During exercise bouts that last for several hours, however, the rate
of liver glucose release more closely matches the muscles’ needs,
keeping plasma glucose at or only slightly above the resting
concentrations. As muscle uptake of glucose increases, the liver’s
rate of glucose release also increases. In most cases, plasma
glucose does not begin to decline until late in the activity as liver
glycogen stores become depleted, at which time the glucagon
concentration increases significantly. Glucagon and cortisol together
enhance gluconeogenesis, providing more fuel.
Figure 4.4 illustrates the changes in plasma concentrations of
epinephrine, norepinephrine, glucagon, cortisol, and glucose during 3
h of cycling. Although the hormonal regulation of glucose remains
intact throughout such long-term activities, the liver’s glycogen supply
may become limiting and the liver’s rate of glucose release may be
unable to keep pace with the muscles’ rate of glucose uptake. Under
this condition, plasma glucose may decline despite strong hormonal
stimulation. Glucose ingestion during the activity can play a major
role in maintaining plasma glucose concentrations.
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FIGURE 4.4 Changes (as a percentage of preexercise values) in plasma concentrations of
epinephrine, norepinephrine, glucagon, cortisol, and glucose during 3 h of cycling at 65%
O2.
Glucose Uptake by Muscle
Merely releasing sufficient amounts of glucose into the blood does not
ensure that the muscle cells will have enough glucose to meet their
energy demands. Not only must the glucose be released and
delivered to these cells, it also must be taken up by the cells.
Transport of glucose through the cell membranes and into muscle
cells is controlled by insulin. Once glucose is delivered to the muscle,
insulin facilitates its transport into the fibers.
Surprisingly, as seen in figure 4.5, plasma insulin concentration
tends to decrease during prolonged exercise, despite a slight
increase in plasma glucose concentration and glucose uptake by
muscle. This apparent contradiction between the plasma insulin
concentrations and the muscles’ need for glucose serves as a
reminder that a hormone’s activity is determined not only by its
concentration in the blood but also by a cell’s sensitivity to that
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hormone. In this case, the cell’s sensitivity to insulin is at least as
important as the concentration of circulating hormone. Exercise may
enhance insulin’s binding to receptors on the muscle fiber, thereby
reducing the need for high concentrations of plasma insulin to
transport glucose across the muscle cell membrane into the cell. This
is important, because during exercise, four hormones are working to
release glucose from its storage sites and create new glucose. High
insulin concentrations would oppose their action, preventing this
needed increase in plasma glucose supply.
FIGURE 4.5 Changes in plasma concentrations of glucose and insulin during prolonged cycling at 65%
to 70% of O2. Note the gradual decline in insulin throughout the exercise, suggesting an increased
sensitivity to insulin during prolonged effort.
CNS–Endocrine System Interaction
The central nervous system (CNS) integrates the activities of the
nervous and endocrine systems. Therefore, it is not surprising that
the CNS is involved in the regulation of carbohydrate metabolism
through the sensing of hormones (especially insulin) and nutrients
(including glucose, fatty acids, and amino acids).
The actions of insulin on the CNS were clarified through studies
using a mouse model of insulin resistance, a condition commonly
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associated with obesity.4 In this model, insulin signaling directly to
neurons in the brain regulated how the tissues elsewhere around the
body regulated glucose metabolism. Other studies have similarly
demonstrated the important regulatory actions of the CNS on insulin’s
control of carbohydrate metabolism throughout the body. In these
studies, the researchers directly injected glucose into areas of the
brain to specifically stimulate receptors sensitive to glucose. Then
they measured the hormones that regulate glucose metabolism as
well as how much glucose was taken up and stored by the liver and
muscle, respectively.7 By injecting glucose into the brain to examine
central signaling and measuring glucose uptake throughout the body,
they were able to show that the brain itself is indeed sensitive to
glucose and helps to control the hormones released throughout the
body in the regulation of carbohydrate metabolism.
Other hormones have a similar integration with the CNS. Leptin is
a hormone that is released by adipose tissue in response to feeding,
suppressing food intake. It also acts through specific CNS neurons
called pro-opiomelanocortin (POMC) neurons to decrease glucose
production in the liver since more glucose is not required after
feeding. Glucagon-like peptide 1 (GLP-1), a hormone released in the
gut that signals β-cells in the pancreas to release insulin, also works
through CNS POMC cells to decrease liver glucose production
through both a decrease in gluconeogenesis and increased
glycogenolysis. The integration of these hormonal effects through the
CNS and subsequent peripheral actions is illustrated in figure 4.6.
Within the brain itself, glucose regulation is particularly important
because glucose is the only substrate that can be used for the brain’s
metabolism. Neuronal activity is tightly coupled with glucose
utilization, and neurons preferentially use glucose derived from
lactate (see chapter 2) as an oxidative fuel source.13 As in exercising
muscle, lactate can be shuttled between cells in the brain to support
oxidative metabolism.8 Together these findings illustrate the important
role of the CNS in regulating hormones associated with carbohydrate
metabolism and glucose homeostasis, both within the CNS and
throughout the body.
Regulation of Fat Metabolism During Exercise
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Free fatty acids are a primary source of energy at rest and during
prolonged endurance exercise. They are derived from triglycerides
through the action of the enzyme lipase, which breaks down
triglycerides into FFA and glycerol. Although fat generally contributes
less than carbohydrate does to muscles’ energy needs during most
bouts of exercise, mobilization and oxidation of FFAs are critical to
performance in endurance exercise. During such prolonged activity,
carbohydrate reserves become depleted, and muscle must rely more
heavily on the oxidation of fat for energy production. When
carbohydrate reserves are low (low plasma glucose and low muscle
glycogen), the endocrine system can accelerate the oxidation of fats
(lipolysis), thus ensuring that muscles’ energy needs can be met.
Free fatty acids are stored as triglycerides in adipose tissue and
within muscle fibers. Adipose tissue triglycerides, once broken down
to release the FFAs, must be transported to the muscle fibers. The
rate of FFA uptake by active muscle correlates highly with the plasma
FFA concentration. Increasing this concentration would increase
cellular uptake of the FFA. Therefore, the rate of triglyceride
breakdown may determine, in part, the rate at which muscles use fat
as a fuel source during exercise.
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FIGURE 4.6 Hormones secreted throughout the peripheral tissues in the body, including the
gastrointestinal tract and the pancreas, stimulate specific receptors in the hypothalamus to control
glucose metabolism in the liver. (a) Insulin released by the β-cells in the pancreas acts through appetitestimulating (NPY/AgRP) neurons in the arcuate nucleus of the hypothalamus. These neurons are
stimulated by the peptide neurotransmitter neuropeptide Y (NPY) and release agouti-related peptide;
insulin receptors are also present on these specialized neurons. (b and c) The pro-opiomelanocortin
(POMC) neurons are stimulated by both leptin and glucagon-like peptide 1 (GLP-1). Together these
hormones act on neurons in the brain, signaling through the vagus nerve to the liver to decrease glucose
production.
Based on Lam et al. (2005).
The rate of lipolysis is controlled by at least five hormones:
(Decreased) insulin
Epinephrine
Norepinephrine
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Cortisol
Growth hormone
The major factor responsible for adipose tissue lipolysis during
exercise is a fall in circulating insulin. Lipolysis is also enhanced
through the elevation of epinephrine and norepinephrine. In addition
to having a role in gluconeogenesis, cortisol accelerates the
mobilization and use of FFAs for energy during exercise. Plasma
cortisol concentration peaks after 30 to 45 min of exercise and then
decreases to near-normal levels. But the plasma FFA concentration
continues to increase throughout the activity, meaning that lipase
continues to be activated by other hormones. The hormones that
continue this process are the catecholamines and GH. The thyroid
hormones also contribute to the mobilization and metabolism of FFAs
but to a much lesser degree.
Thus, the endocrine system plays a critical role in regulating ATP
production during exercise as well as controlling the balance between
carbohydrate and fat metabolism.
In Review
Plasma glucose concentration is increased by the combined actions of glucagon,
epinephrine, norepinephrine, and cortisol. These hormones promote
glycogenolysis and gluconeogenesis, thus increasing the amount of glucose
available for use as a fuel source. This is important during exercise, particularly
long-duration or high-intensity exercise, when blood glucose concentrations might
otherwise decline.
Insulin allows circulating glucose to enter the cells, where it can be used for
energy production. But insulin concentrations decline during prolonged exercise,
indicating that exercise increases cell sensitivity to insulin so that less of the
hormone is required during exercise than at rest.
When carbohydrate reserves are low, the body turns more to fat oxidation for
energy and lipolysis increases. This process is facilitated by a decreased insulin
concentration and increased concentrations of epinephrine, norepinephrine,
cortisol, and GH.
Hormonal Regulation of Fluid and Electrolytes
During Exercise
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Fluid balance during exercise is critical for optimal metabolic,
cardiovascular, and thermoregulatory function. At the onset of
exercise, water shifts from the plasma volume to the interstitial and
intracellular spaces. This water shift is specific to the amount of
muscle that is active and the intensity of effort. Metabolic by-products
begin to accumulate in and around the muscle fibers, increasing the
osmotic pressure there. Water then moves passively into these areas
by diffusion. Also, increased muscular activity increases blood
pressure, which in turn drives water out of the blood (hydrostatic
forces). In addition, sweating increases during exercise. The
combined effect of these actions is that plasma volume decreases.
For example, prolonged running at approximately 75% of O2max
decreases plasma volume by 5% to 10%. Reduced plasma volume
can decrease blood pressure and increase the strain on the heart to
pump blood to the working muscles. Both of these effects can impede
athletic performance.
Endocrine Glands Involved in Fluid and Electrolyte
Homeostasis
The endocrine system plays a major role in monitoring fluid levels
and electrolyte balance, especially that of sodium. The two major
endocrine glands involved in these processes are the posterior
pituitary and the adrenal cortex. Additionally, the kidneys not only
serve as the primary target organ for hormones released by these
glands but also function as endocrine glands themselves.
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Posterior Pituitary
The pituitary’s posterior lobe is an outgrowth of neural tissue from the
hypothalamus. For this reason, it is also referred to as the
neurohypophysis. It secretes two hormones: antidiuretic hormone
(ADH)—also called vasopressin or arginine vasopressin—and
oxytocin. Both of these hormones are actually produced in the
hypothalamus, travel through nerves, and are stored in vesicles
within nerve endings in the posterior pituitary. These hormones are
released into capillaries as needed in response to neural impulses
from the hypothalamus.
Of the two posterior pituitary hormones, only ADH is known to play
an important role during exercise. Antidiuretic hormone promotes
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water conservation by increasing water reabsorption by the kidneys.
As a result, less water is excreted in the urine, creating an
“antidiuresis.”
Muscular activity and sweating cause electrolytes to become
concentrated in the blood plasma as more fluid, compared to
electrolytes, leaves the plasma. This is called hemoconcentration,
and it increases the plasma osmolality. Osmolality refers to the ionic
concentration of dissolved substances in the plasma. The presence
of dissolved molecules and minerals in various body fluid
compartments (i.e., intracellular, plasma, and interstitial spaces)
generates an osmotic pressure or attraction to retain water within a
compartment. The amount of osmotic pressure exerted by a body
fluid is proportional to the number of molecular particles (osmoles, or
Osm) in solution. A solution that has 1 Osm of solute dissolved in
each kilogram (the weight of a liter) of water is said to have an
osmolality of 1 osmole per kilogram (1 Osm/kg), whereas a solution
that has 0.001 Osm/kg has an osmolality of 1 milliosmole per
kilogram (1 mOsm/kg). Normally, body fluids have an osmolality of
300 mOsm/kg. Increasing the osmolality of the solutions in one body
compartment generally causes water to be drawn away from adjacent
compartments that have a lower osmolality (i.e., more water).
An increased plasma osmolality is the primary physiological
stimulus for ADH release. The increased osmolality is sensed by
osmoreceptors in the hypothalamus. A second and related stimulus
for ADH release is a low plasma volume sensed by baroreceptors in
the cardiovascular system. In response to either stimulus, the
hypothalamus sends neural impulses to the posterior pituitary,
stimulating ADH release. The ADH enters the blood, travels to the
kidneys, and promotes water retention in an effort to dilute the plasma
electrolyte concentration back to normal levels. This hormone’s role in
conserving body water minimizes the extent of water loss and
therefore the risk of severe dehydration during periods of heavy
sweating and hard exercise. Figure 4.7 illustrates this process.
Adrenal Cortex
A group of hormones called mineralocorticoids, secreted from the
adrenal cortex, maintain electrolyte balance, especially that of sodium
(Na+) and potassium (K+), in the extracellular fluids. Aldosterone is
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the major mineralocorticoid, responsible for at least 95% of all
mineralocorticoid activity. It works primarily by promoting renal
reabsorption of sodium, thus causing the body to retain sodium.
When sodium is retained, so is water, which follows the osmotic
gradient; thus, aldosterone, like ADH, results in water retention.
Sodium retention also enhances potassium excretion, so aldosterone
plays a role in potassium balance as well. For these reasons,
aldosterone secretion is stimulated by many factors, including
decreased plasma sodium, decreased blood volume, decreased
blood pressure, and increased plasma potassium concentration.
FIGURE 4.7 The mechanism by which antidiuretic hormone (ADH) helps to conserve body water.
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The Kidneys as Endocrine Organs
Although the kidneys are not typically considered major endocrine
organs, they do release two important hormones. The kidneys play a
role in determining the aldosterone concentration in the blood. While
the primary regulator of aldosterone release is plasma electrolyte
concentration, a second set of hormones also determines
aldosterone concentration and thus helps regulate body fluid balance.
In response to a fall in blood pressure or plasma volume, blood flow
to the kidneys decreases. Stimulated by activation of the sympathetic
nervous system, the kidneys release renin. Renin is an enzyme that
is released into the circulation, where it converts a molecule called
angiotensinogen to angiotensin I. Angiotensin I is subsequently
converted to its active form, angiotensin II, in the lungs with the aid of
an enzyme, angiotensin-converting enzyme (ACE). Angiotensin II
stimulates aldosterone release from the adrenal cortex for sodium
and water resorption at the kidneys. Figure 4.8 shows the mechanism
involved in renal control of blood pressure, the renin-angiotensinaldosterone mechanism. In addition to stimulating aldosterone
release from the adrenal cortex, angiotensin II causes blood vessels
to constrict. Because ACE catalyzes the conversion of angiotensin I
to angiotensin II, ACE inhibitors are sometimes prescribed for
individuals with hypertension, since relaxation of the blood vessels
lowers blood pressure.
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FIGURE 4.8 Water loss from plasma during exercise leads to a sequence of events that promotes
sodium (Na+) and water reabsorption from the renal tubules, thereby reducing urine production. In the
hours after exercise when fluids are consumed, the elevated aldosterone concentration causes an
increase in the extracellular volume and an expansion of plasma volume.
Recall that aldosterone’s primary action is to promote sodium
reabsorption in the kidneys. Because water follows sodium, this renal
conservation of sodium causes the kidneys to also retain water. The
net effect is to conserve the body’s fluid content, thereby minimizing
the loss of plasma volume while keeping blood pressure near normal.
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Figure 4.9 illustrates the changes in plasma volume and aldosterone
concentrations during 2 h of exercise. The hormonal influences of
ADH and aldosterone persist for up to 48 h after exercise, reducing
urine production and protecting the body from further dehydration.
The kidneys also release a hormone called erythropoietin.
Erythropoietin (EPO) regulates red blood cell (erythrocyte)
production by stimulating bone marrow cells. The red blood cells are
essential for transporting oxygen to the tissues and removing carbon
dioxide, so this hormone is extremely important in our adaptation to
training and altitude.
Most athletes involved in heavy training have an expanded plasma
volume, which dilutes various blood constituents. As proteins leave
working muscle, they reenter the plasma through the lymphatic
system, and water follows. This is a relatively short-term
phenomenon, and new protein synthesis eventually supports this
expanded plasma volume. During the early phases of plasma volume
expansion, however, hemoglobin concentration decreases; that is, a
hemodilution occurs.
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FIGURE 4.9 Changes in plasma volume and aldosterone concentration during 2 h of cycling exercise.
Note that plasma volume declines rapidly during the first few minutes of exercise and then shows a
smaller rate of decline despite large sweat losses. Plasma aldosterone concentration, on the other hand,
increases rather steadily throughout the exercise.
The actual amount of hemoglobin has not changed; it is simply
diluted. For this reason, some athletes who actually have normal
hemoglobin concentrations may appear to be anemic as a
consequence of Na+-induced hemodilution. This condition, not to be
confused with true anemia, can be remedied with a few days of rest,
allowing time for aldosterone concentrations to return to normal and
for the kidneys to unload the extra Na+ and water.
In Review
Loss of fluid (plasma) from the blood results in a concentration of the constituents
of the blood, a phenomenon referred to as hemoconcentration. Conversely, a gain
of fluid in the blood results in a dilution of the constituents of the blood, which is
referred to as hemodilution.
The presence of dissolved particles in body fluid compartments generates an
osmotic pressure or attraction to retain water. The osmotic pressure is
proportional to the number of molecular particles in solution. A solution that has 1
osmole of solute dissolved in each kilogram (the weight of a liter) of water is said
to have an osmolality of 1 osmole per kilogram (1 Osm/kg).
Body fluids normally have an osmolality of 300 mOsm/kg. Increasing the
osmolality of the solutions in one body compartment generally causes water to be
drawn away from adjacent compartments.
The two primary hormones involved in the regulation of fluid balance are ADH and
aldosterone.
Antidiuretic hormone is released in response to increased plasma osmolality.
When osmoreceptors in the hypothalamus sense this increase, the hypothalamus
triggers ADH release from the posterior pituitary. Low blood volume is a
secondary stimulus for ADH release.
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Antidiuretic hormone acts on the kidneys, directly promoting water reabsorption
and thus fluid conservation. As more fluid is resorbed, plasma volume increases
and plasma osmolality decreases.
When plasma volume or blood pressure decreases, the kidneys release an
enzyme called renin that converts angiotensinogen into angiotensin I, which later
becomes angiotensin II in the lung circulation. Angiotensin II is a powerful
constrictor of blood vessels and increases peripheral resistance, increasing the
blood pressure.
Angiotensin II also triggers the release of aldosterone from the adrenal cortex.
Aldosterone promotes sodium reabsorption in the kidneys, which in turn causes
water retention, thus minimizing the loss of plasma volume.
Hormonal Regulation of Caloric Intake
The regulation of appetite, the sensations of hunger and satiety, and
the feeling of fullness are part of a complex system that involves
hormonal signaling from all over the body, including the
gastrointestinal system and fat cells. Food intake is primarily under
the control of the hypothalamus with some input from higher brain
centers. The satiety area of the brain is located in the ventromedial
nucleus, while the hunger center is located in the lateral
hypothalamus. The hypothalamus, as it does for many aspects of
homeostasis, integrates neural and hormonal signals for both the
short- and long-term regulation of eating behavior and calorie intake.
Hormones that influence these brain centers are synthesized in,
and released from, peripheral tissues including the gut and fat cells
(adipocytes). These hormones can be categorically split into those
that are anorexigenic, meaning that they suppress appetite, and
those that are orexigenic, meaning that they stimulate appetite. The
main hormones that regulate appetite and satiety are cholecystokinin,
leptin, peptide YY, GLP-1, insulin, and ghrelin.
Gastrointestinal Tract Hormones
Short-term control of food intake is regulated by plasma
concentrations of nutrients including amino acids, glucose, and lipids.
However, another significant influence on short-term regulation of
food intake involves hormones released in the gastrointestinal (GI)
tract. Gastrointestinal distention caused by a full stomach triggers the
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release of the hormone cholecystokinin (CCK), which stimulates
afferent fibers of the vagus nerve to send signals to the brain to
suppress hunger. In addition, other hormones including GLP-1 and
peptide YY (PYY) are secreted from the large and small intestines
during and after eating. These hormones travel through the blood to
the brain where they suppress hunger. Peptide YY also acts on the
hypothalamus to inhibit gastric motility. Insulin released from the
pancreas in response to eating also acts as a satiety hormone.
RESEARCH PERSPECTIVE 4.2
Endurance Training for More Red Blood Cells
The direct association between endurance training and increased red blood
cell volume was first discovered in 1949.6 This adaptation to endurance
training, called erythropoiesis, increases oxygen delivery to the exercising
muscle by increasing the number of red blood cells available to carry oxygen
in addition to increasing the blood volume pumped with every beat of the
heart. Increasing red blood cell volume is a fundamental component of the
increase in aerobic capacity (maximal oxygen uptake) that occurs with regular
endurance exercise training (discussed further in chapter 11). Although
erythropoiesis is a central mechanism by which endurance training
adaptations occur, relatively little is known about how red blood cell volume
expansion is regulated during repeated bouts of endurance training.
A recent study conducted in Switzerland examined erythropoiesis and its
physiological regulators during an 8-week endurance-training program in a
group of healthy young men and women.12 Researchers measured body
composition, heart rate, blood pressure, maximal exercise capacity, total blood
volume, red blood cell volume, and erythropoietin (a hormone that stimulates
red blood cell production) concentrations in the blood throughout the 8-week
training period. At the end of the training period, average red blood cell volume
had doubled and maximal exercise capacity had increased by ~10%. Across
the 8 weeks of training, total blood volume increased during week 2 and
remained high throughout; erythropoietin also increased in week 2 but
subsequently returned to baseline values by week 4. Red blood cell volume
was increased by week 4 and continued to increase through week 8, coming
after the preceding increases in blood volume and circulating erythropoietin
concentration. By week 8, exercise-induced increases in erythropoietin
concentration had ended but red blood cell volume continued to increase,
suggesting that there are still unexplained mechanisms that control
erythropoiesis. These findings provided novel insight into the time course of
expansion of red blood cell volume as an adaptation to endurance training,
while at the same time uncovering new questions for future research.
271
Conversely, the hormone ghrelin is secreted from the stomach and
pancreas when the stomach is empty; it can be thought of as a
hunger hormone. Ghrelin is transmitted through the blood to the
brain where it crosses the blood–brain barrier to act on the hunger
areas in the lateral hypothalamus. After eating, ghrelin concentrations
decrease.
Adipose Tissue as an Endocrine Organ
In addition to hormones secreted by the stomach and intestines to
signal hunger or fullness, additional hormones are secreted by
adipocytes (fat cells) that likewise act on the hunger and satiety
centers in the hypothalamus. Because the level of these hormones
depends on the amount of adipose tissue in the body, which changes
slowly, these hormones are more involved in the long-term regulation
of food intake. The hormone leptin is primarily secreted by fat cells
and acts on receptors in the hypothalamus to decrease hunger.
Leptin is also an indicator of energy balance, as its circulating
concentrations are proportional to body fat. A simple schematic of
how leptin and ghrelin interact to modify appetite and satiety is
presented in figure 4.10.
A great deal has been discovered about what leptin does in terms
of energy balance from a mouse model using mice that lack the
ability to make leptin in their fat cells. These mice have a voracious
appetite and are massively obese. In obese humans, circulating
concentrations of leptin are elevated, but many obese humans are
leptin resistant. This suggests that despite an elevated signal that
they are in an overfed state, the signal is not being transmitted
through the hypothalamus to initiate the sensations of satiety.
Interestingly, obese humans also appear to have a dampened ghrelin
signal. Researchers are only beginning to understand how hormonal
appetite signaling changes with weight gain and obesity. This is
critical in order to determine how best to treat obesity, as well as how
exercise may influence appetite and satiety hormones.
272
FIGURE 4.10 Hormonal regulation of appetite and satiety by ghrelin and leptin. Acting through specific
hypothalamic receptors (GH secretagogue receptor, or GHS-r, for ghrelin and obesity receptor, or Ob-r,
for leptin), ghrelin increases, and leptin decreases, appetite.
RESEARCH PERSPECTIVE 4.3
Does Environmental Temperature Alter the Hormones
That Control Appetite?
The interactions among exercise, appetite, and energy intake are important for
the control and maintenance of energy homeostasis and body weight.
Scientifically, these interactions have received widespread attention because
they may hold the key to treating excess weight gain and obesity. Leptin and
ghrelin are hormones that regulate the perception of hunger and lead to
changes in appetite. Leptin (the “satiety hormone”) decreases energy intake,
while ghrelin (the “hunger hormone”) increases energy intake. Both exercise
and exposure to extreme temperatures can affect the concentrations of these
273
appetite-regulating hormones. Circulating ghrelin concentration and perception
of hunger both decrease immediately after a single bout of moderate- to highintensity exercise but have no influence on the total energy intake throughout
the day. Environmental temperature has an impact on resting metabolic rate.
Indigenous populations who live in polar climates have elevated basal
metabolic rates, while those who live in tropical climates have decreased
basal metabolic rates. Additionally, exercise in a hot environment reduces
appetite, while exercise in the cold stimulates appetite; however, it is unknown
if these effects involve changes in circulating leptin or ghrelin.
Recently, a group of researchers at the University of Nebraska Omaha
conducted an experiment to examine how exercise in different environmental
temperatures would affect the leptin and ghrelin responses to exercise.9
Research subjects completed three separate 1 h bouts of cycling in hot (33 °C
[91°F]), neutral (20 °C [68 °F]), and cold (7 °C [45 °F]) air temperatures. The
research team measured leptin and ghrelin in blood samples collected
preexercise, immediately postexercise, and after a 3 h recovery. Similar to
previous studies, circulating leptin was increased immediately after exercise
and remained elevated 3 h later. Circulating ghrelin concentrations did not
change. Although the researchers hypothesized that there would be larger
increases in leptin after exercise in the heat and larger increases in ghrelin
after exercise in the cold, there was no effect of air temperature on any
hormone measurements. The conclusion from this study was that
environmental temperature does not alter the leptin or ghrelin responses to
short bouts of aerobic exercise. Future research studies are needed to
determine what other variables might affect regulatory hormone and hunger
responses following exercise in extreme environments.
Effects of Acute and Chronic Exercise on Satiety Hormones
Acute bouts of moderate- to vigorous-intensity exercise temporarily
suppress appetite, likely by decreasing ghrelin and increasing GLP-1
and PYY released from the GI tract.14 These hormonal changes are
most pronounced with aerobic exercise and are not observed after
resistance exercise training.3
With chronic exercise training comes a shift in energy balance due
to the calorie deficit induced by exercise. This is accompanied by a
partial compensation to increase hunger and therefore caloric intake
through changes in the appetite-regulating hormones. Several studies
have observed an increase in plasma PYY concentrations after
exercise training, which would be consistent with improved satiety.
Counterintuitively, the hunger hormone ghrelin does not change in
people who do not lose weight during exercise training but increases
274
significantly in those who do lose weight.10 In general, appetite and
satiety hormones are sensitive to the total energy balance that is
modulated by regular exercise. It has been suggested that for elite
athletes who need to monitor their energy balance, measures of
circulating leptin and ghrelin may help to determine when the athlete
is overtraining and may help predict states of energy deficit.5
275
IN CLOSING
In this chapter, we focused on the role of the endocrine system in regulating
some of the many physiological processes that accompany exercise. We
discussed the role of hormones in regulating the metabolism of glucose and fat
for energy metabolism and the role of other hormones in maintaining fluid
balance. We touched on some of the relatively new findings about how
hormones regulate appetite and calorie consumption. We next look at the
related topics of energy expenditure and fatigue during exercise.
KEY TERMS
adrenaline
aldosterone
angiotensin-converting enzyme (ACE)
antidiuretic hormone (ADH)
autocrines
catecholamines
cholecystokinin (CCK)
cortisol
cyclic adenosine monophosphate (cAMP)
direct gene activation
downregulation
epinephrine
erythropoietin (EPO)
ghrelin
glucagon
glucocorticoids
growth hormone (GH)
hemoconcentration
hemodilution
hormone
hyperglycemia
hypoglycemia
inhibiting factors
insulin
insulin resistance
insulin sensitivity
leptin
mineralocorticoids
nonsteroid hormones
276
osmolality
prostaglandins
releasing factors
renin
renin-angiotensin-aldosterone mechanism
second messenger
steroid hormones
target cells
thyrotropin (TSH)
thyroxine (T4)
triiodothyronine (T3)
upregulation
STUDY QUESTIONS
1.
2.
What is an endocrine gland, and what are the functions of hormones?
3.
How can hormones have very specific functions when they reach nearly all
parts of the body through the blood?
4.
What determines plasma concentrations of specific hormones? What
determines their effectiveness on target cells and tissues?
5.
Define the terms upregulation and downregulation. How do target cells
become more or less sensitive to hormones?
6.
What are second messengers, and what role do they play in hormonal
control of cell function?
7.
Briefly outline the major endocrine glands, their hormones, and the specific
action of these hormones.
8.
Which of the hormones outlined in question 7 are of major significance
during exercise?
9.
What hormones are involved in the regulation of metabolism during
exercise? How do they influence the availability of carbohydrates and fats
for energy during exercise lasting for several hours?
10.
Discuss how the central nervous system helps integrate glucose regulation
and the hormones involved in this process.
11.
12.
Describe the hormonal regulation of fluid balance during exercise.
Explain the difference between steroid hormones and nonsteroid hormones
in terms of their actions at target cells.
Discuss the sources and function of the hormones cholecystokinin, leptin,
and ghrelin, and explain how they are interrelated.
277
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
278
279
5
Energy Expenditure, Fatigue, and
Muscle Soreness
In this chapter and in the web study guide
Measuring Energy Expenditure
Direct Calorimetry
Indirect Calorimetry
Isotopic Measurements of Energy Metabolism
ACTIVITY 5.1 Evaluating Energy Use explores six methods of measuring energy use and the
advantages and disadvantages of each.
Energy Expenditure at Rest and During Exercise
Basal and Resting Metabolic Rates
Metabolic Rate During Submaximal Exercise
Maximal Capacity for Aerobic Exercise
Anaerobic Effort and Exercise Capacity
Economy of Effort
Characteristics of Successful Athletes in Aerobic Endurance Events
Energy Cost of Various Activities
AUDIO FOR FIGURE 5.3 describes the relationship between oxygen uptake and power output during
exercise.
AUDIO FOR FIGURE 5.4 describes the relationship between exercise intensity and oxygen uptake in a
trained and an untrained subject.
ACTIVITY 5.2 Energy Expenditure at Rest and During Exercise reviews the measurement of basal
metabolic rate and the common terms used to refer to the best single measurement of
cardiorespiratory endurance and aerobic fitness.
ANIMATION FOR FIGURE 5.5 breaks down the concepts of oxygen deficit and EPOC.
AUDIO FOR FIGURE 5.7 describes the effect of running economy.
Fatigue and Its Causes
Energy Systems and Fatigue
280
Metabolic By-Products and Fatigue
Neuromuscular Fatigue
Other Contributors to Fatigue
AUDIO FOR FIGURE 5.8 describes the relationship between subjective fatigue and muscle glycogen
concentration.
AUDIO FOR FIGURE 5.10 describes the use of muscle glycogen in various leg muscles during
running.
AUDIO FOR FIGURE 5.12 describes changes in muscle pH during sprint exercise and recovery.
ACTIVITY 5.3 Sources of Fatigue Affecting Athletic Performance considers various sources of fatigue
and how they affect athletic performance.
Critical Power: The Link Between Energy Expenditure and
Fatigue
AUDIO FOR FIGURE 5.13 describes the concept of critical power.
Muscle Soreness and Muscle Cramps
Acute Muscle Soreness
Delayed-Onset Muscle Soreness
Exercise-Induced Muscle Cramps
VIDEO 5.1 presents Mike Bergeron on the two types of muscle cramping and the best ways to prevent
muscle cramps.
ACTIVITY 5.4 Muscle Soreness and Cramps investigates the causes and treatment of muscle
soreness and muscle cramps.
In Closing
281
T
he causes and sites of what exercisers and athletes call “fatigue” are as
numerous as the sensations that characterize it. Although it is usually considered in
terms of how different parts of the body feel—burning lungs, aching legs, unyielding
tiredness—researchers have begun to focus on the role the brain plays in fatigue.
After all, the brain collects all of the sensory feedback from the body and
determines when physical exertion simply cannot continue. Recent research has
shown that a fatigued brain can squash successful sport performance as much as
tired muscles can. An article by Dr. Samuele Marcora titled “Mental Fatigue Impairs
Physical Performance in Humans,” published in the Journal of Applied Physiology,
suggests that perceptions of fatigue cause us to reach our physical limits long
before the body does. A group of rugby players exercised to fatigue during an
endurance test but were subsequently able to do a 5 s sprint. That is, the brain’s
perceptions of fatigue stopped the endurance trial before the athletes had reached
their physical limits. The brain may be acting as a regulatory brake, slowing down
activity before a somatic limit is reached. This does not mean that fatigue is
imagined. Rather, its causes are complex (for example, both the muscles and the
brain rely on glucose and glycogen for fuel).
One cannot understand exercise physiology without understanding
some key concepts about energy expenditure at rest and during
exercise. In chapter 2, we discussed the formation of adenosine
triphosphate (ATP), the major form of chemical energy stored within,
and used by, cells. Adenosine triphosphate is produced from
substrates by a series of processes that are known collectively as
metabolism. In the first half of this chapter we discuss various
techniques for measuring the whole-body energy expenditure or
metabolic rate, then we describe how energy expenditure varies
from basal or resting conditions up to maximal exercise intensities. If
exercise is sustained for a prolonged time, eventually muscular
contraction cannot be sustained and performance will diminish. This
inability to maintain muscle contractions is broadly called fatigue.
Fatigue is a complex, multidimensional phenomenon that may or
may not result from an inability to maintain metabolism and expend
energy. Because fatigue often has a metabolic component, it is
discussed in this chapter along with energy expenditure. Muscle
282
soreness and cramping are also discussed as additional factors that
can limit exercise.
Measuring Energy Expenditure
The energy used by contracting muscle fibers during exercise cannot
be directly measured. But numerous laboratory methods can be
used to calculate whole-body energy expenditure at rest and during
exercise. Several of these methods have been in use since the early
1900s. Others are new and have only recently been used in exercise
physiology.
Direct Calorimetry
Only about 40% of the energy liberated during the metabolism of
glucose and fats is used to produce ATP. The remaining 60% is
converted to heat, so one way to gauge the rate and quantity of
energy production is to measure the body’s heat production. This
technique is called direct calorimetry (“measuring heat”), since the
basic unit of heat is the calorie (cal).
This approach was first described by Zuntz and Hagemann in the
late 1800s.29 They developed the calorimeter, which consists of an
insulated, airtight chamber as illustrated in figure 5.1. The walls of
the chamber contain tubing through which water is circulated. In the
chamber, the heat produced by the body radiates to the walls and
warms the water. The water temperature and temperature changes
of the air entering and leaving the chamber vary with the heat the
body generates. One’s metabolism can be calculated from the
resulting values.
Calorimeters are expensive to construct and operate and are slow
to generate results, so very few are in actual operation. Their only
real advantage is that they measure heat directly, but they have
several disadvantages for exercise physiology. Although a
calorimeter can provide an accurate measure of total body energy
expenditure over time, it cannot follow rapid changes in energy
expenditure. Therefore, while direct calorimetry is useful for
measuring resting metabolism and energy expended during
prolonged, steady-state aerobic exercise, energy metabolism during
more typical exercise situations cannot be adequately studied with a
283
direct calorimeter. Second, exercise equipment such as a motordriven treadmill gives off its own heat that must be accounted for in
the calculations. Third, not all heat is liberated from the body; some
is stored in the body, causing body temperature to rise. And finally,
sweating affects the measurements and the constants used in the
calculations of heat produced. Consequently, it is easier and less
expensive to quantify energy expenditure by measuring the
exchange of oxygen and carbon dioxide that occurs during oxidative
phosphorylation.
Indirect Calorimetry
As discussed in chapter 2, oxidative metabolism of glucose and fat—
the main substrates for aerobic exercise—uses O2 and produces
CO2 and water. The rate of O2 and CO2 exchanged in the lungs
normally equals the rate of their usage and release by the body
tissues. Based on this principle, energy expenditure can be
determined by measuring the respiratory exchange of O2 and CO2.
This method of estimating total body energy expenditure is called
indirect calorimetry because heat production is not measured
directly.
284
FIGURE 5.1 A direct calorimeter for the measurement of energy expenditure by an exercising human
subject. The heat generated by the subject’s body is transferred to the air and walls of the chamber
(through conduction, convection, and evaporation). This heat produced by the subject—a measure of
his or her metabolic rate—is measured by recording the temperature change in the air entering and
leaving the calorimeter as well as in the water flowing through its walls.
In order for oxygen consumption to reflect energy metabolism
accurately, energy production must be almost completely oxidative. If
a large portion of energy is being produced anaerobically, respiratory
gas measurements will not reflect all metabolic processes and will
underestimate the total energy expenditure. Therefore, this
technique is limited to steady-state aerobic activities lasting a few
minutes or longer, which fortunately takes into account most daily
activities including exercise.
Respiratory gas exchange is determined through measurement of
the volume of O2 and CO2 that enters and leaves the lungs during a
given period of time. Because O2 is removed from the inspired air in
the alveoli and CO2 is added to the alveolar air, the expired O2
concentration is less than the inspired, whereas the CO2
concentration is higher in expired air than in inspired air.
Consequently, the differences in the concentrations of these gases
between the inspired and the expired air tell us how much O2 is
being taken up and how much CO2 is being produced by the body.
Because the body has only limited O2 storage, the amount taken up
at the lungs accurately reflects the body’s use of O2. Although a
number of sophisticated and expensive methods are available for
measuring the respiratory exchange of O2 and CO2, the simplest and
oldest methods (i.e., Douglas bag to collect expired air and chemical
analysis of collected gas sample) are probably the most accurate,
but they are relatively slow and permit only a few measurements
during each session. Modern electronic computer systems for
respiratory gas exchange measurements offer the ability to make
rapid and repeated measurements.
Notice in figure 5.2 that the gas expired by the subject passes
through a hose into a mixing chamber. The subject is wearing a nose
clip so that all expired gas is collected from the mouth and none is
lost to the air. From the mixing chamber, samples are pumped to
electronic oxygen and carbon dioxide analyzers. In this setup, a
285
computer uses the measurements of expired gas (air) volume and
the fraction (percentage) of oxygen and carbon dioxide in a sample
of that expired air to calculate O2 uptake and CO2 production.
Sophisticated equipment can do these calculations breath by breath,
but calculations are more typically done over discrete time periods
lasting from one to several minutes.
Calculating Oxygen Consumption and Carbon Dioxide
Production
Using equipment like that shown in figure 5.2, exercise physiologists
can measure the three variables needed to calculate the actual
volume of oxygen consumed (VO2) and volume of CO2 produced
(VCO2). Generally, values are presented as oxygen consumed per
minute ( O2) and CO2 produced per minute ( CO2). The dot over
the V ( ) indicates the rate of O2 consumption or CO2 production per
minute.
In simplified form, O2 is equal to the volume of O2 inspired minus
the volume of O2 expired. To calculate the volume of O2 inspired, we
multiply the volume of air inspired by the fraction of that air that is
composed of O2; the volume of O2 expired is equal to the volume of
air expired multiplied by the fraction of the expired air that is
composed of O2. The same holds true for CO2.
286
FIGURE 5.2 Typical equipment that is routinely used by exercise physiologists to measure O2
consumption and CO2 production. These values can be used to calculate O2max and the respiratory
exchange ratio and therefore energy expenditure. Although this equipment is cumbersome and limits
movement, smaller versions have recently been adapted for use under a variety of conditions in the
laboratory, on the playing field, in industry, and elsewhere.
Thus, calculation of
information:
O2 and
CO2 requires the following
Volume of air inspired ( I)
Volume of air expired ( E)
Fraction of oxygen in the inspired air (F1O2)
Fraction of CO2 in the inspired air (F1CO2)
Fraction of oxygen in the expired air (FEO2)
Fraction of CO2 in the expired air (FECO2)
The oxygen consumption, in liters of oxygen consumed per minute,
can then be calculated as follows:
O2 = (
I
× F1O2) − (
287
E
× FEO2)
The CO2 production is similarly calculated as follows:
CO2 = (
E
× FECO2) − (
I
× F1CO2)
These equations provide reasonably good estimates of O2 and
CO2. However, the equations are based on the idea that inspired air
volume exactly equals expired air volume and there are no changes
in gases stored within the body. Since there are differences in gas
storage during exercise (discussed next), more accurate equations
can be derived from the variables listed.
Haldane Transformation
Over the years, scientists have attempted to simplify the actual
calculation of oxygen consumption and CO2 production. Several of
the measurements needed in the preceding equations are known
and do not change. The gas concentrations of the three gases that
make up inspired air are known: oxygen accounts for 20.93% (or
0.2093), CO2 accounts for 0.03% (0.0003), and nitrogen accounts for
79.03% (0.7903) of the inspired air. What about the volume of
inspired and expired air? Aren’t they the same, such that we would
need to measure only one of the two?
Inspired air volume equals expired air volume only when the
volume of O2 consumed equals the volume of CO2 produced. When
the volume of oxygen consumed is greater than the volume of CO2
produced, I is greater than E. Likewise, E is greater than I
when the volume of CO2 produced is greater than the volume of
oxygen consumed. However, the one thing that is constant is that the
volume of nitrogen inspired ( I N2) is equal to the volume of nitrogen
expired ( E N2). Because I N2 = I × FI N2 and E N2 = E × FE N2,
we can calculate I from E by using the following equation, which
has been referred to as the Haldane transformation:
(1)
I
× FI N2 =
E
× FE N2,
which can be rewritten as
(2)
I
=(
E
× FE N2) / FI N2.
Furthermore, because we are actually measuring the concentrations
of O2 and CO2 in the expired gases, we can calculate FEN2 from the
288
sum of FEO2 and FECO2, or
(3) FEN2 = 1 − (FEO2 + FECO2).
So, in pulling all of this information together, we can rewrite the
equation for calculating O2 as follows:
O2 = (
I
× FIO2) − (
E
× FEO2)
By substituting equation 2, we get the following:
O2 = [(
E
× FE N2) / (FI N2 × FIO2)] − [(
) × (FEO2)]
E
By substituting known values for FIO2 of 0.2093 and for FIN2 of
0.7903, we get the following:
O2 = [(
E
× FEN2) / (0.7903 × 0.2093)] − (
E
× FEO2)
By substituting equation 3, we get the following:
O2 = {(
) × [1 − (FEO2 + FECO2)] × (0.2093 / 0.7903)} − (
FEO2)
E
E
×
or, simplified,
O2 = (
) × {[1 − (FEO2 + FECO2)] × 0.265} − (
E
E
× FEO2)
or, further simplified,
O2 = (
) × {[1 − (FEO2 + FECO2)] × 0.265} − (FEO2).
E
This final equation is the one actually used in practice by exercise
physiologists, although computers now do the calculating
automatically in most laboratories.
One final correction is necessary. When air is expired, it is at body
temperature (BT), is at the prevailing atmospheric or ambient
pressure (P), and is saturated (S) with water vapor, or what are
referred to as BTPS conditions. Each of these influences would not
only add error to the measurement of O2 and CO2 but also would
make it difficult to compare measurements made in laboratories at
different altitudes, for example. For that reason, every gas volume is
routinely converted to its standard temperature (ST: 0 °C or 273 K)
and pressure (P: 760 mmHg), dry equivalent (D), or STPD. This is
accomplished by a series of correction equations.
Respiratory Exchange Ratio
289
To estimate the amount of energy used by the body, it is necessary
to know the type of food substrate (combination of carbohydrate, fat,
protein) being oxidized. The carbon and oxygen contents of glucose,
free fatty acids (FFAs), and amino acids differ dramatically. As a
result, the amount of oxygen used during metabolism depends on
the type of fuel being oxidized. Indirect calorimetry measures the
rate of CO2 release ( CO2) and oxygen consumption ( O2). The
ratio between these two values is termed the respiratory exchange
ratio (RER).
RER =
CO2 /
O2
In general, the amount of oxygen needed to completely oxidize a
molecule of carbohydrate or fat is proportional to the amount of
carbon in that fuel. For example, glucose (C6H12O6) contains six
carbon atoms. During glucose combustion, six molecules of oxygen
are used to produce 6 CO2 molecules, 6 H2O molecules, and 32 ATP
molecules:
6 O2 + C6H12O6 → 6 CO2 + 6 H2O + 32 ATP
By evaluating how much CO2 is released compared with the amount
of O2 consumed, we find that the RER is 1.0:
RER =
CO2 /
O2 = 6 CO2 / 6 O2 = 1.0
As shown later in the chapter, the RER value varies with the type
of fuels being used for energy. Free fatty acids have considerably
more carbon and hydrogen but less oxygen than glucose. Consider
palmitic acid, C16H32O2. To completely oxidize this molecule to CO2
and H2O requires 23 molecules of oxygen:
Ultimately, this oxidation results in 16 molecules of CO2, 16
molecules of H2O, and 129 molecules of ATP:
290
C16H32O2 + 23 O2 → 16 CO2 + 16 H2O + 129 ATP
Combustion of this fat molecule requires significantly more oxygen
than combustion of a carbohydrate molecule. During carbohydrate
oxidation, approximately 6.3 molecules of ATP are produced for
each molecule of O2 used (32 ATP per 6 O2), compared with 5.6
molecules of ATP per molecule of O2 during palmitic acid metabolism
(129 ATP per 23 O2).
Although fat provides more energy than carbohydrate, more
oxygen is needed to oxidize fat than carbohydrate. This means that
the RER value for fat is substantially lower than for carbohydrate.
For palmitic acid, the RER value is 0.70:
RER =
CO2 /
O2 = 16 / 23 = 0.70
Once the RER value is determined from the calculated respiratory
gas volumes, the value can be compared with a table (table 5.1) to
determine the food mixture being oxidized. If, for example, the RER
value is 1.0, the cells are using only glucose or glycogen, and each
liter of oxygen consumed would generate 5.05 kcal. The oxidation of
only fat would yield 4.69 kcal/L of O2, and the oxidation of protein
would yield 4.46 kcal/L of O2 consumed. Thus, if the muscles were
using only glucose and the body were consuming 2 L of O2/min, then
the rate of heat energy production would be 10.1 kcal/min (2 L/min ·
5.05 kcal/L).
Limitations of Indirect Calorimetry
While indirect calorimetry is a common and extremely important tool
of exercise physiologists, it has some limitations. Calculations of gas
exchange assume that the body’s O2 content remains constant and
that CO2 exchange in the lung is proportional to its release from the
cells. Arterial blood remains almost completely oxygen saturated
(about 98%), even during intense effort, and we can accurately
assume that the oxygen being removed from the air we breathe is in
proportion to its cellular uptake. Carbon dioxide exchange, however,
is less constant. Body CO2 pools are quite large and can be altered
simply by deep breathing or by performance of highly intense
exercise. Under these conditions, the amount of CO2 released in the
lung may not represent that being produced in the tissues, so
291
calculations of carbohydrate and fat used based on gas
measurements are accurate only at rest or during steady-state
exercise.
Use of the RER can also lead to inaccuracies. Recall that protein
is not completely oxidized in the body. This makes it impossible to
calculate the body’s protein use from the RER. As a result, the RER
is sometimes referred to as nonprotein RER because it simply
ignores any protein oxidation. Traditionally, protein was thought to
contribute little to the energy used during exercise, so exercise
physiologists felt justified in using the nonprotein RER when making
calculations. But more recent evidence suggests that in exercise
lasting for several hours, protein may contribute up to 5% of the total
energy expended under certain circumstances.
TABLE 5.1 Respiratory Exchange Ratio (RER) as a Function
of Energy Derived From Various Fuel Mixtures
% Kcal from
Carbohydrates
Fats
RER
Energy (kcal/L O2)
0
16
33
51
68
84
100
100
84
67
49
32
16
0
0.71
0.75
0.80
0.85
0.90
0.95
1.00
4.69
4.74
4.80
4.86
4.92
4.99
5.05
The body normally uses a combination of fuels. Respiratory
exchange ratio values vary depending on the specific mixture being
oxidized. At rest, the RER value is typically in the range of 0.78 to
0.80. During exercise, though, muscles rely increasingly on
carbohydrate for energy, resulting in a higher RER. As exercise
intensity increases, the muscles’ carbohydrate demand also
increases. As more carbohydrate is used, the RER value
approaches 1.0.
This increase in the RER value to 1.0 reflects the demands on
blood glucose and muscle glycogen, but it also may indicate that
more CO2 is being unloaded from the blood than is being produced
by the muscles. At or near exhaustion, lactate accumulates in the
blood. The body tries to reverse this acidification by releasing more
CO2. Lactate accumulation increases CO2 production because
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excess acid causes carbonic acid in the blood to be converted to
CO2. As a consequence, the excess CO2 diffuses out of the blood
and into the lungs for exhalation, increasing the amount of CO2
released. For this reason, RER values approaching 1.0 may not
accurately estimate the type of fuel being used by the muscles.
Another complication is that glucose production from the
catabolism of amino acids and fats in the liver produces an RER
below 0.70. Thus, calculations of carbohydrate oxidation from the
RER value will be underestimated if energy is derived from this
process.
Despite its shortcomings, indirect calorimetry still provides the
best estimate of energy expenditure at rest and during aerobic
exercise and is widely used in laboratories throughout the world.
Isotopic Measurements of Energy Metabolism
In the past, determining an individual’s total daily energy expenditure
depended on recording food intake over several days and measuring
body composition changes during that period. This method, although
widely used, is limited by the individual’s ability to keep accurate
records and by the ability to match the individual’s activities to
accurate energy costs.
Fortunately, the use of chemical isotopes has expanded our ability
to investigate energy metabolism. Isotopes are elements with an
atypical atomic weight. They can be either radioactive
(radioisotopes) or nonradioactive (stable isotopes). As an example,
carbon-12 (12C) has a molecular weight of 12, is the most common
natural form of carbon, and is nonradioactive. In contrast, carbon-14
(14C) has two more neutrons than 12C, giving it an atomic weight of
14. 14C is radioactive.
Carbon-13 (13C) constitutes about 1% of the carbon in nature and
is used frequently for studying energy metabolism. Because 13C is
nonradioactive, it is less easily traced within the body than 14C. But
although radioactive isotopes are easily detected in the body, they
pose a hazard to body tissues and thus are used infrequently in
human research.
13C and other isotopes such as hydrogen-2 (deuterium, or 2H) are
used as tracers, meaning that they can be selectively followed in the
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body. Tracer techniques involve infusing isotopes into an individual
and then following their distribution and movement.
Although the method was first described in the 1940s, studies that
used doubly labeled water for monitoring energy expenditure during
normal daily living in humans were not conducted until the 1980s.
The subject ingests a known amount of water labeled with two
isotopes (2H2 and 18O), hence the term doubly labeled water. The
deuterium (2H) diffuses throughout the body’s water, and the oxygen18 (18O) diffuses throughout both the water and the bicarbonate
stores (where much of the CO2 derived from metabolism is stored).
The rate at which the two isotopes leave the body can be determined
by analysis of their presence in a series of urine, saliva, or blood
samples. These turnover rates then can be used to calculate how
much CO2 is produced, and that value can be converted to energy
expenditure through the use of calorimetric equations.
Because isotope turnover is relatively slow, energy metabolism
must be measured for several weeks. Thus, this method is not well
suited for measurements of acute exercise metabolism. However, its
accuracy (more than 98%) and low risk make it well suited for
determining day-to-day energy expenditure.
In Review
Direct calorimetry involves a large sophisticated chamber that directly measures
heat produced by the body; while it can provide very accurate measures of
resting metabolism, it is not a commonly used tool for exercise physiologists.
Indirect calorimetry involves measuring whole-body O2 consumption and CO2
production from expired gases. Since we know the fraction of O2 and CO2 in the
inspired air, three additional measurements are needed: the volume of air
inspired ( I) or expired ( E), the fraction of oxygen in the expired air (FEO2), and
the fraction of CO2 in the expired air (FECO2).
By calculating the RER (the ratio of CO2 production to O2 consumption) and
determining the metabolic substrates being oxidized, we can convert O2 into
energy expenditure in kilocalories.
The RER value at rest is usually 0.78 to 0.80. The RER value for the oxidation of
fat is 0.70 and is 1.00 for carbohydrates.
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Isotopes can be used to determine metabolic rate over longer periods of time.
They are injected or ingested into the body. The rates at which they are cleared
can be used to calculate CO2 production and then caloric expenditure.
Energy Expenditure at Rest and During
Exercise
With the techniques described in the previous section, exercise
physiologists can measure the amount of energy a person expends
in a variety of conditions. This section deals with the body’s rates of
energy expenditure (metabolic rates) at rest, during submaximal and
maximal exercise, and during the period of recovery following an
acute exercise bout.
Basal and Resting Metabolic Rates
The rate at which the body uses energy is called the metabolic rate.
Estimates of energy expenditure at rest and during exercise are
often based on measurement of whole-body oxygen consumption (
O2) and its caloric equivalent. At rest, an average person consumes
about 0.3 L of O2/min.
Knowing an individual’s O2 allows us to calculate that person’s
caloric expenditure. Recall that at rest, the body usually burns a
mixture of carbohydrate and fat. An RER value of approximately 0.80
is fairly common for most resting individuals eating a mixed diet. The
caloric equivalent associated with an RER value of 0.80 is 4.80 kcal
per liter of O2 consumed (see table 5.1). Using these values and an
estimate of 0.3 L of O2/min, we can calculate this individual’s caloric
expenditure as follows:
kcal/day = liters of O2 consumed per day × kcal used per liter of O2
= 432 L O2/day × 4.80 kcal/L O2
= 2,074 kcal/day
This value closely agrees with the average resting energy
expenditure expected for a 70 kg (154 lb) man. Of course, it does not
include the extra energy needed for normal daily activity or any
excess energy used for exercise.
One standardized measure of energy expenditure at rest is the
basal metabolic rate (BMR). The BMR is the rate of energy
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expenditure for an individual at rest in a supine position, measured in
a thermoneutral environment immediately after at least 8 h of sleep
and at least 12 h of fasting. This value reflects the minimum amount
of energy required to carry on essential physiological functions.
Because muscle has high metabolic activity, the BMR is directly
related to an individual’s fat-free mass and is generally reported in
kilocalories per kilogram of fat-free mass per minute (kcal · kg FFM−1
· min−1). The higher the fat-free mass, the more total calories
expended in a day. Because women tend to have a lower fat-free
mass and a greater percent body fat than men, women tend to have
a lower BMR than men of a similar weight.
Body surface area also affects BMR. The higher the surface area,
the more heat loss occurs from the skin, which raises the BMR
because more energy is needed to maintain body temperature. For
this reason, the BMR is sometimes reported in kcal per square meter
of body surface area per hour (kcal · m−2 · h−1). Because we are
discussing daily energy expenditure, we will use the simpler unit,
kcal/day.
Many other factors affect BMR, including these:
Age: BMR gradually decreases with increasing age,
generally because of a decrease in fat-free mass.
Body temperature: BMR increases with increasing
temperature.
Psychological stress: Stress increases activity of the
sympathetic nervous system, which increases the BMR.
Hormones: For example, increased release of thyroxine from
the thyroid gland or epinephrine from the adrenal medulla
can both increase the BMR.
Instead of BMR, most researchers measure resting metabolic rate
(RMR), which is similar to BMR but does not require the stringent
standardized conditions associated with a true BMR. Basal
metabolic rate and RMR values are typically within 5% to 10% of
each other, with BMR slightly lower, and range from 1,200 to 2,400
kcal/day. But the average total metabolic rate of an individual
engaged in normal daily activity ranges from 1,800 to 3,000 kcal.
However, the energy expenditure for large athletes engaged in
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intense training—for example, large football players in two-a-day
practice sessions—can exceed 10,000 kcal/day!
Metabolic Rate During Submaximal Exercise
Exercise increases the energy requirement well in excess of RMR.
Metabolism increases in direct proportion to the increase in exercise
intensity, as shown in figure 5.3a. As this subject exercised on a
cycle ergometer for 5 min at 50 watts (W), oxygen consumption (
O2) increased from its resting value to a steady-state value within 1
min or so. The same subject then cycled for 5 min at 100 W, and
again a steady-state O2 was reached in 1 to 2 min. In a similar
manner, the subject cycled for 5 min at 150 W, 200 W, 250 W, and
300 W, respectively, and steady-state values were achieved at each
power output. The steady-state O2 value represents the energy
cost for that specific power output. The steady-state O2 values
were plotted against their respective power outputs (right half in
figure 5.3a), showing clearly that there is a linear increase in the O2
with increases in power output.
From more recent studies, it is clear that the O2 response at
higher rates of work does not follow the steady-state response
pattern shown in figure 5.3a but rather looks more like the graphs
presented in figure 5.3b. At power outputs above the lactate
threshold (the lactate response is indicated by the dashed line in the
right half of figure 5.3, a and b), the oxygen consumption continues
to increase beyond the typical 1 to 2 min needed to reach a steadystate value. This increase has been called the slow component of
oxygen uptake kinetics.11 The most likely mechanism for this slow
component is an alteration in muscle fiber recruitment patterns, with
the recruitment of more type II muscle fibers, which are less efficient
(i.e., they require a higher O2 to achieve the same power output).11
A similar, but unrelated, phenomenon is referred to as the O2
drift, defined as a slow increase in
O2 during prolonged,
submaximal, constant power output exercise. Unlike the slow
component, O2 drift is observed at power outputs well below
lactate threshold, and the increase in O2 drift is more gradual.
Although not understood completely, O2 drift is likely attributable to
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an increase in ventilation and effects of increased circulating
catecholamines.
Maximal Capacity for Aerobic Exercise
In figure 5.3a, it is clear that when the subject cycled at 300 W, the
O2 response was not different from that achieved at 250 W. This
indicates that the subject had reached the maximal limit of his ability
to increase his O2. This value is referred to as aerobic capacity,
maximal oxygen uptake ( O2max). O2max is widely regarded as the
best single measurement of cardiorespiratory endurance or
aerobic fitness. This concept is further illustrated in figure 5.4, which
compares the O2max of a trained and an untrained man.
In some exercise settings, as intensity increases, a subject
reaches volitional fatigue before a plateau occurs in the
O2
response (the criterion for a true O2max). In such cases, the highest
oxygen uptake achieved is more correctly termed the peak oxygen
uptake ( O2peak). For example, a highly trained marathon runner will
almost always achieve a higher O2 value ( O2max) on a treadmill
than when he or she is tested to volitional fatigue on a cycle
ergometer ( O2peak). In the latter case, fatigue of the quadriceps
muscles is likely to occur before a true maximal oxygen uptake is
achieved.
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FIGURE 5.3 The increase in oxygen uptake with increasing power output (a) as originally proposed
by P.-O. Åstrand and K. Rodahl, Textbook of work physiology: Physiological bases of exercise, 3rd ed.
(New York: McGraw-Hill, 1986), p. 300; and (b) as redrawn by Gaesser and Poole (1996, p. 36). See
the text for a detailed explanation of this figure.
Reprinted by permission from G.A. Gaesser and D.C. Poole, “The Slow Component of Oxygen Uptake Kinetics in
Humans,” Exercise and Sport Sciences Reviews 24 (1996): 36.
Although O2max is a good measure of aerobic fitness, the winner
of a marathon race cannot be predicted from the runner’s laboratory-
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measured O2max. This suggests that while a relatively high O2max
is a necessary attribute for elite endurance athletes, a stellar
endurance athlete requires more than a high O2max, a concept
discussed in chapter 11.
Also, research has documented that O2max typically increases
with physical training for only 8 to 12 weeks and then plateaus
despite continued higher-intensity training. Although O2max does not
continue to increase, participants continue to improve their
endurance performance. It appears that these individuals develop
the ability to perform at a higher percentage of their O2max. Welltrained marathon runners, for example, can complete a 42 km (26.1
mi) marathon at an average pace that equals approximately 75% to
80% of their O2max or higher.
FIGURE 5.4 The relation between exercise intensity (running speed) and oxygen uptake, illustrating
O2max in a trained and an untrained man.
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Consider the case of Alberto Salazar, arguably the premier
marathon runner in the world in the 1980s. His measured O2max
was 70 ml · kg−1 · min−1. That is below the O2max one might expect
based on his best marathon performance of 2 h 8 min. He was,
however, able to run at a race pace in the marathon at 86% of his
O2max, a percentage considerably higher than that of other worldclass runners. This may partly explain his world-class running ability.
Because individuals’ energy requirements vary with body size,
O2max generally is expressed relative to body weight, in milliliters of
oxygen consumed per kilogram of body weight per minute (ml · kg−1
· min−1). This allows a more accurate comparison of the
cardiorespiratory endurance capacity of different-sized individuals
who exercise in weight-bearing events, such as running. In
nonweight-bearing activities, such as swimming and cycling,
endurance is better reflected by O2max measured in liters per
minute.
Normally active but untrained 18- to 22-year-old college students
have an average O2max of about 38 to 42 ml · kg−1 · min−1 for
women and 44 to 50 ml · kg−1 · min−1 for men. In contrast, poorly
conditioned adults may have values below 20 ml · kg−1 · min−1. At the
other end of the spectrum, O2max values of 80 to 84 ml · kg−1 · min−1
have been measured for elite male long-distance runners and crosscountry skiers. (The highest O2max value recorded for a man is that
of a champion Norwegian cross-country skier who had a O2max of
94 ml · kg−1 · min−1! The highest value recorded for a woman is 77 ml
· kg−1 · min−1 for a Russian cross-country skier.)
After the age of 25 to 30 years, the O2max of inactive individuals
decreases at a rate of about 1% per year, attributable to the
combination of biological aging and sedentary lifestyle. Two
physiological reasons why adult women generally have
O2max
values considerably below those of adult men (discussed further in
chapter 19) are sex differences in body composition (women
generally have less fat-free mass and more fat mass) and blood
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hemoglobin content (lower in women, so they have a lower oxygencarrying capacity).
Anaerobic Effort and Exercise Capacity
No exercise is 100% aerobic or 100% anaerobic. The methods we
have discussed thus far ignore the anaerobic processes that
accompany aerobic exercise. How can the interaction of the aerobic
(oxidative) processes and the anaerobic processes be evaluated?
The most common methods for estimating anaerobic contribution to
sustained exercise involve examination of either the excess
postexercise oxygen consumption (EPOC) or the lactate threshold.
Postexercise Oxygen Consumption
The matching of energy requirements during exercise with oxygen
delivery is not perfect. When aerobic exercise begins, the oxygen
transport system (respiration and circulation) does not immediately
supply the needed quantity of oxygen to the active muscles. Oxygen
consumption requires several minutes to reach the required (steadystate) level at which the aerobic processes are fully functional, even
though the body’s oxygen requirements increase the moment
exercise begins.
Because oxygen needs and oxygen supply differ during the
transition from rest to exercise, the body incurs an oxygen deficit,
as shown in figure 5.5. This deficit accrues even at low exercise
intensities. The oxygen deficit is calculated simply as the difference
between the oxygen required for a given exercise intensity (steady
state) and the actual oxygen consumption. Despite the insufficient
oxygen delivery at the onset of exercise, the active muscles are able
to generate the ATP needed through the anaerobic pathways
described in chapter 2.
During the initial minutes of recovery, even though active muscle
activity has stopped, oxygen consumption does not immediately
decrease to a resting value. Rather, oxygen consumption decreases
gradually toward resting values (figure 5.5). This excess oxygen
consumption, which exceeds that required at rest, was traditionally
referred to as the “oxygen debt.” The more common term today is
excess postexercise oxygen consumption (EPOC). The EPOC is
the volume of oxygen consumed during the minutes immediately
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after exercise ceases that is above that normally consumed at rest.
Everyone has experienced this phenomenon at the end of an intense
exercise bout: A fast climb up several flights of stairs leaves one with
a rapid pulse and breathing hard, physiological adjustments that
serve to support the EPOC. After several minutes of recovery, heart
rate and breathing return to resting rates.
FIGURE 5.5 Oxygen requirement (dashed line) and oxygen consumption (red solid line) during
exercise and recovery, illustrating the oxygen deficit and the concept of excess postexercise oxygen
consumption (EPOC).
For many years, the EPOC curve was described as having two
distinct components: an initial fast component and a secondary slow
component. According to classical theory, the fast component of the
curve represented the oxygen required to rebuild the ATP and
phosphocreatine (PCr) used during the initial stages of exercise.
Without sufficient oxygen available, the high-energy phosphate
bonds in these compounds were broken to supply the required
energy. During recovery, these bonds would need to be re-formed,
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via oxidative processes, to replenish the energy stores or to repay
the debt. The slow component of the curve was thought to result
from removal of accumulated lactate from the tissues, by either
conversion to glycogen or oxidation to CO2 and H2O, thus providing
the energy needed to restore glycogen stores.
According to this theory, both the fast and slow components of the
curve reflected the anaerobic activity that had occurred during
exercise. The belief was that by examining the postexercise oxygen
consumption, one could estimate the amount of anaerobic activity
that had occurred.
However, more recently researchers have concluded that the
classical explanation of EPOC is too simplistic. For example, during
the initial phase of exercise, some oxygen is borrowed from the
oxygen stores (hemoglobin and myoglobin), and that oxygen must
be replenished during early recovery as well. Also, respiration
remains temporarily elevated following exercise partly in an effort to
clear CO2 that has accumulated in the tissues as a by-product of
metabolism. Body temperature also is elevated, which keeps the
metabolic and respiratory rates high, thus requiring more oxygen;
and elevated concentrations of norepinephrine and epinephrine
during exercise have similar effects.
Thus, the EPOC depends on many factors other than merely the
replenishing of ATP and PCr and the clearing of lactate produced by
anaerobic metabolism.
Lactate Threshold
Many investigators consider the lactate threshold a good indicator of
an athlete’s potential for endurance exercise. The lactate threshold
is defined as the point at which blood lactate begins to substantially
accumulate above resting concentrations during exercise of
increasing intensity. For example, a runner might be required to run
on the treadmill at different speeds with a rest between each speed.
After each run, a blood sample is taken and blood lactate is
measured. Figure 5.6 depicts the relation between blood lactate and
running velocity. At low running velocities, blood lactate
concentrations remain near resting levels. But as running speed
increases, the blood lactate concentration increases rapidly beyond
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some threshold exercise intensity. The point at which blood lactate
first appears to increase disproportionately above resting values is
called the lactate threshold.
FIGURE 5.6 The relation between exercise intensity (running velocity) and blood lactate
concentration. Blood samples were taken from a runner’s arm vein and analyzed for lactate after the
subject ran at each speed for 5 min. LT = lactate threshold.
The lactate threshold has been thought to reflect the interaction of
the aerobic and anaerobic energy systems. Some researchers have
suggested that the lactate threshold represents a significant shift
toward anaerobic glycolysis, which forms lactate from pyruvic acid.
Consequently, the sudden increase in blood lactate with increasing
effort has also been referred to as the anaerobic threshold. However,
blood lactate concentration is determined not only by the production
of lactate in skeletal muscle or other tissues but also by the
clearance of lactate from the blood by the liver and its use as a fuel
source by muscle and other tissues in the body. Thus, lactate
threshold is best defined as that point in time during exercise of
increasing intensity when the rate of lactate production exceeds the
rate of lactate clearance.
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The lactate threshold is usually expressed as the percentage of
maximal oxygen uptake (% O2max) at which it occurs. In untrained
people, the lactate threshold typically occurs at approximately 50%
to 60% of their O2max, while elite endurance athletes may not reach
lactate threshold until closer to 70% or 80% of O2max.
From the previous section, we learned that in addition to a high
O2max, the percentage of O2max that an athlete can maintain for a
prolonged period is a major determinant of successful endurance
performance. The lactate threshold is likely the major determinant of
the fastest pace that can be tolerated during a long-term endurance
event. So the ability to perform at a higher percentage of O2max
probably reflects a higher lactate threshold. Consequently, a lactate
threshold at 80%
O2max suggests a greater aerobic exercise
tolerance than a threshold at 60%
O2max. Generally, in two
individuals with the same maximal oxygen uptake, the person with
the highest lactate threshold usually exhibits the best endurance
performance, although other factors contribute as well, including
economy of movement.
Economy of Effort
As people become more skilled at performing an exercise, the
energy demands during exercise at a given pace are reduced. In a
sense, people become more economical. (Note that we avoid calling
this efficiency, which has a more stringent mechanical definition.)
This is illustrated in figure 5.7 by the data from two distance runners.
At all running speeds faster than 11.3 km/h (7.0 mph), runner B used
significantly less oxygen than runner A. These men had similar
O2max values (64-65 ml · kg−1 · min−1), so runner B’s lower
submaximal energy use would be a decided advantage during
competition.
These two runners competed on numerous occasions. During
marathon races, they ran at paces requiring them to use 85% of their
O2max. On average, runner B beat runner A by 13 min in their
competitions. Because their O2max values were so similar but their
energy needs so different during these events, much of runner B’s
competitive advantage could be attributed to his greater running
306
economy. Unfortunately, there is no single specific explanation for
the underlying causes of differences in economy, which are likely
due to a variety of complex physiological and biomechanical factors.
FIGURE 5.7
The oxygen requirements for two distance runners running at various speeds. Although
they had similar O2max values (64-65 ml · kg−1 · min−1), runner B was more economical and therefore
could run at a faster pace for a given oxygen cost.
Various studies with sprint, middle-distance, and distance runners
have shown that marathon runners are generally very economical. It
is not uncommon for ultra-long-distance runners to use 5% to 10%
less energy than middle-distance runners and sprinters at a given
pace. However, this economy of effort has been studied at only
relatively slow speeds (paces of 10-19 km/h, or 6-12 mph). We can
307
reasonably assume that distance runners are less economical at
sprinting than runners who train specifically for short, faster races. It
is probable that runners self-select their chosen events in part
because they achieve early success, success achieved in part due
to better running economy at that distance.
Variations in running form and the specificity of training for sprint
and distance running may account for at least part of these
differences in running economy. Film analyses reveal that middledistance runners and sprinters have significantly more vertical body
movement when running at 11 to 19 km/h (7-12 mph) than
marathoners do. But such speeds are well below those required
during middle-distance races and probably do not accurately reflect
the running economy of competitors in shorter events of 1,500 m (1
mi) or less.
Performance in other athletic events might be even more affected
by economy of movement. Part of the energy expended during
swimming, for example, is used to support the body on the surface of
the water and to generate enough force to overcome the water’s
resistance to motion. Although the energy needed for swimming
depends on body size and buoyancy, the efficient application of force
against the water is the major determinant of swimming economy.
Characteristics of Successful Athletes in Aerobic Endurance
Events
From our discussion of the metabolic characteristics of aerobic
endurance athletes in this chapter and of their muscle fiber type
characteristics in chapter 1, it is clear that to be successful in aerobic
endurance activities, one needs some combination of the following:
High O2max
High lactate threshold when expressed as a percentage of
O2max
High economy of effort, or a low O2 for a given absolute
exercise intensity
High percentage of type I muscle fibers
From the limited data available, these four characteristics appear
to be properly ranked in their order of importance. As an example,
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running velocity at lactate threshold and
O2max are the best
predictors of actual race pace among a group of elite distance
runners. However, each of those runners already has a high O2max,
which, in elite athletes, is supported by having a large heart and an
expanded blood volume. Although economy of effort is important, it
does not vary much between elite runners. Finally, having a high
percentage of type I muscle fibers is helpful but not essential. The
bronze medal winner in one of the Olympic marathon races had only
50% type I muscle fibers in his gastrocnemius muscle, one of the
primary muscles used in running.
Energy Cost of Various Activities
The amount of energy expended for different activities varies with
the intensity and type of exercise. Despite subtle differences in
economy, the average energy costs of many activities have been
determined, usually through the measurement of oxygen
consumption during the activity to determine an average oxygen
uptake per unit of time. The amount of energy expended per minute
(kcal/min) then can be calculated from this value.
These values typically ignore the anaerobic aspects of exercise
and the EPOC. This omission is important because an activity that
costs a total of 300 kcal during the actual exercise period may cost
an additional 100 kcal during the recovery period. Thus, the total
cost of that activity would be 400, not 300, kcal. Because of these
nuances along with individual variation, the “calories burned”
readouts on exercise machines can be highly inaccurate.
The body requires 0.16 to 0.35 L of oxygen per minute to satisfy
its resting energy requirements. This would amount to 0.80 to 1.75
kcal/min, 48 to 105 kcal/h, or 1,152 to 2,520 kcal/day. Obviously, any
activity above resting levels will add to the projected daily
expenditure. The range for total daily caloric expenditure is highly
variable and depends on
physical activity (by far the largest influence),
age,
sex,
body size,
309
weight, and
body composition.
The energy costs of sport activities also differ. Some, such as
archery or bowling, require only slightly more energy than rest.
Others, such as sprinting, require such a high rate of energy delivery
that they can be maintained for only seconds. Clearly, both exercise
intensity and duration of the activity must be considered to determine
energy expended. For example, approximately 29 kcal/min is
expended during running at 25 km/h (15.5 mph), but this pace can
be endured for only brief periods. Jogging at 11 km/h (7 mph), on the
other hand, expends only 14.5 kcal/min, half that of running at 25
km/h (15.5 mph). But jogging can be maintained for considerably
longer, resulting in greater total energy expenditure for an exercise
session.
Table 5.2 provides estimates of average energy expenditure
during various activities for men and women. Remember that these
values are merely averages, and these figures vary considerably
with individual differences such as those on the preceding list and
with individual skill (economy of movement).
In Review
The basal metabolic rate (BMR) is the minimum amount of energy required by
the body to sustain basic cellular functions and is related to fat-free body mass
and, to a lesser extent, body surface area. It typically ranges from 1,100 to 2,500
kcal/day, but when daily activity is added, typical daily caloric expenditure is
1,700 to 3,100 kcal/day.
O2 increases linearly with increased exercise intensity but eventually reaches a
plateau. Its maximal value is called the O2max. When volitional fatigue limits
exercise before a true maximum is reached, the term O2peak is used.
Successful aerobic performance is linked to a high O2max, to the ability to
perform for long periods at a high percentage of O2max, to the running velocity
at lactate threshold, and to a good economy of movement.
The EPOC is the elevated metabolic rate above resting levels that occurs during
the recovery period immediately after exercise has ceased.
Lactate threshold is that point at which blood lactate production begins to exceed
the body’s ability to clear lactate, resulting in a rapid increase in blood lactate
310
concentration during exercise of increasing intensity. Generally, individuals with
higher lactate thresholds, expressed as a percentage of their
O2max, are
capable of better endurance performances. Lactate threshold is a strong
determinant of an athlete’s optimal pace in endurance events such as distance
running and cycling.
TABLE 5.2 Average Values for Energy Expenditure During
Various Physical Activities
Activity
Men (kcal/min)
Women (kcal/min)
Relative to body mass (kcal · kg−1 · min−1)
Basketball
Cycling
11.3 km/h (7.0 mph)
16.1 km/h (10.0 mph)
Handball
Running
12.1 km/h (7.5 mph)
16.1 km/h (10.0 mph)
Sitting
Sleeping
Standing
Swimming (crawl),
4.8 km/h (3.0 mph)
Tennis
Walking, 5.6 km/h (3.5 mph)
Weightlifting
Wrestling
8.6
6.8
0.123
5.0
7.5
11.0
3.9
5.9
8.6
0.071
0.107
0.157
14.0
18.2
1.7
1.2
1.8
20.0
11.0
14.3
1.3
0.9
1.4
15.7
0.200
0.260
0.024
0.017
0.026
0.285
7.1
5.0
8.2
13.1
5.5
3.9
6.4
10.3
0.101
0.071
0.117
0.187
Note. The values presented are for a 70 kg (154 b) man and a 55 kg (121 lb) woman. These values will
vary depending on individual differences.
Fatigue and Its Causes
The term fatigue means different things to different people.
Sensations that exercising individuals describe as fatigue are
markedly different for a 400 m (437 yd) runner (an event lasting 45 to
60 s) than for a marathoner nearing the end of a 42.2 km (26.2 mi)
endurance event. Therefore, it is not surprising that the causes of
fatigue are different in those two scenarios as well. In exercise
physiology, we typically describe fatigue as decrements in muscular
performance with continued effort accompanied by general
sensations of tiredness. An alternative definition used in research
studies to quantify fatigue is the inability to maintain the required
power output to continue muscular work at a given intensity. The fact
that fatigue is reversible by rest distinguishes it from muscle
weakness or damage (discussed later in the chapter).
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RESEARCH PERSPECTIVE 5.1
Energy Expenditure of Walking
Understanding how much metabolic energy is expended during walking has
many applications, from clinical rehabilitation programs to fitness and activity
tracking and even military maneuvers. The metabolic energy required for
walking can be accurately determined by directly measuring oxygen
consumption during activity. However, this measurement technique is
impractical outside the laboratory. Published equations that predict this
energy requirement are frequently used. The two most established and
commonly used equations are those developed by the American College of
Sports Medicine (ACSM)1 and by a group of research scientists at the U.S.
Army Research Institute of Environmental Medicine (USARIEM).21 Both of
these equations are specific to body mass and divide the person’s metabolic
rate into resting and nonresting components, where the nonresting
component is speed dependent. Although these equations are considered
the gold standards for predicting energy expenditure during walking, they
were developed based on studies that included only young, healthy, male
subjects of a relatively similar body size.
A recent study conducted at Southern Methodist University in Dallas,
Texas, derived a new mathematical model to predict the metabolic energy
requirements of walking.15 Data from 10 previous studies were compiled to
create a data set of over 400 subjects of both sexes who varied in age,
height, body weight, and fitness level. Researchers then developed
mathematical models to identify the variables required for accurate
predictions of metabolic energy requirements across this heterogeneous
subject pool and found that the most accurate predictions accounted for the
walker’s height (ht), a variable that is absent in the commonly used
equations. Like previous equations, that accuracy of the prediction was
increased when the walking metabolism was quantified as two separate
components, the minimum walking component (different from the resting
component) and the velocity-dependent component. The study resulted in a
new model for predicting metabolic energy expenditure that predicted over
90% of the actual metabolic cost across all walking speeds:
O2 total = ( O2 rest + 3.85) + (5.97 · v2/ht)
where walking velocity (v) is measured in m/s, ht in m, and O2 in ml O2 ·
kg−1 · min−1. In this equation, ( O2 rest + 3.85) is the minimum walking
energy expenditure, (5.97 · v2/ht) is the velocity- and height-dependent
energy expenditure, and [3.85 + (5.97 · v2/ht)] quantifies the total walking
component.
This model can now be used to inform exercise prescriptions for
numerous health and fitness outcomes in wide-ranging populations.
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Ask most exercisers what causes fatigue during exercise, and the
most common two-word answer is “lactic acid.” Not only is this
common misconception an oversimplification but also there is
mounting evidence that lactic acid has beneficial effects on exercise
performance (see chapter 2). Fatigue is an extremely complex
phenomenon, and its causes can range from the molecular level to
the entire body. Most efforts to describe the underlying causes and
sites of fatigue have focused on
a decreased rate of energy delivery (ATP-PCr, anaerobic
glycolysis, and oxidative metabolism);
accumulation of metabolic by-products, such as lactate and
H+;
failure of the muscle fiber’s contractile mechanism; and
alterations in neural control of muscle contraction.
The first three causes occur within the muscle itself; along with
alterations in motor nerve control of muscle function, these are often
referred to as peripheral fatigue. In addition to alterations at the
motor unit level, changes in the brain or central nervous system may
also cause what has become known as central fatigue.
However, none of these alone can explain all aspects or all types
of fatigue, and several causes may act synergistically to bring about
fatigue. Mechanisms of fatigue depend on the type and intensity of
the exercise, the fiber type of the involved muscles, the subject’s
training status, and even his or her diet. Many questions about
fatigue remain unanswered, including the cellular sites of fatigue
within the muscle fibers themselves. It is important to remember that
while fatigue arises at least in part from failure of cross-bridge
cycling within the muscle cells, this machinery depends on the
nervous, cardiovascular, and energy systems to support it.14 Fatigue
is rarely caused by a single factor but typically by multiple factors
acting synergistically at multiple sites. Some potential sites of fatigue
are discussed next.
Energy Systems and Fatigue
The energy systems are an obvious area to explore when one is
considering possible causes of fatigue. When we feel fatigued, we
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often express this by saying, “I have no energy.” But this use of the
term energy is far removed from its physiological meaning. What role
does energy availability play in fatigue during exercise, in the true
physiological sense of providing ATP from substrates?
PCr Depletion
Recall that PCr is used for short-term high-intensity effort, to rebuild
ATP as it is used and thus to maintain ATP stores within the muscle.
Biopsy studies of human thigh muscles have shown that during
repeated maximal contractions, fatigue coincides with PCr depletion.
Although ATP is directly responsible for the energy used during such
activities, it is depleted less rapidly than PCr during muscular effort
because ATP is being produced by other systems (see figure 2.6).
But as PCr is depleted, the ability to quickly replace the spent ATP is
hindered. Use of ATP continues, but the ATP-PCr system is less able
to replace it. Thus, ATP concentration also decreases. At
exhaustion, both ATP and PCr may be depleted.
To delay fatigue, an athlete must control the rate of effort through
proper pacing to ensure that PCr and ATP are not prematurely
exhausted. This holds true even in endurance-type events. If the
beginning pace is too rapid, available ATP and PCr concentrations
will quickly decrease, leading to early fatigue and an inability to
maintain the pace in the event’s later stages. Training and
experience allow the athlete to judge the optimal pace that permits
the most efficient use of ATP and PCr for the entire event.
Glycogen Depletion
Muscle ATP concentrations are also maintained by the breakdown of
muscle glycogen. In events lasting longer than a few seconds,
muscle glycogen becomes the primary energy source for ATP
synthesis. Unfortunately, glycogen reserves are limited and are
depleted quickly. Since the muscle biopsy technique was first
established, studies have shown a correlation between muscle
glycogen depletion and fatigue during prolonged exercise.
Muscle glycogen is used more rapidly during the first few minutes
of exercise than in the later stages, as seen in figure 5.8.6 The
illustration shows the change in muscle glycogen content in the
subject’s gastrocnemius (calf) muscle during the test. Although the
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subject ran the test at a steady pace, the rate of muscle glycogen
metabolized from the gastrocnemius was greatest during the first 75
min.
FIGURE 5.8 (a) The decline in gastrocnemius (calf) muscle glycogen during 3 h of treadmill running at
70% of O2max, and (b) the subject’s subjective rating of the effort. Note that the effort was rated as
moderate for nearly 1.5 h of the run, although glycogen was decreasing steadily. Not until the muscle
glycogen became quite low (less than 50 mmol/kg) did the rating of effort increase.
Adapted by permission from D.L. Costill, Inside Running: Basics of Sports Physiology (Indianapolis: Benchmark
Press, 1986). Copyright 1986 Cooper Publishing Group, Carmel, IN.
The subject also reported his perceived exertion (how difficult his
effort seemed to be) at various times during the test. He felt only
moderately stressed early in the run, when his glycogen stores were
still high, even though he was using glycogen at a high rate. He did
not perceive severe fatigue until his muscle glycogen levels were
nearly depleted. Thus, the sensation of fatigue in long-term exercise
coincides with a decreased concentration of muscle glycogen but not
with its rate of depletion. Marathon runners commonly refer to the
sudden onset of fatigue that they experience at 29 to 35 km (18-22
mi) as “hitting the wall.” At least part of this sensation can be
attributed to muscle glycogen depletion.
Glycogen Depletion in Different Fiber Types
Muscle fibers are recruited and deplete their energy reserves in
selected patterns. The individual fibers most frequently recruited
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during exercise may become depleted of glycogen. This reduces the
number of fibers capable of producing the muscular force needed for
exercise.
This glycogen depletion is illustrated in figure 5.9, which shows a
micrograph of muscle fibers taken from a runner after a 30 km (18.6
mi) run. Figure 5.9a has been stained to differentiate type I and type
II fibers. One of the type II fibers is circled. Figure 5.9b shows a
second sample from the same muscle, stained to show glycogen.
The redder (darker) the stain, the more glycogen is present. Before
the run, all fibers were full of glycogen and appeared red (not
depicted). In figure 5.9b (after the run), the lighter type I fibers are
almost completely depleted of glycogen. This suggests that type I
fibers are used more heavily during endurance exercise that requires
only moderate force development, such as the 30 km run.
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FIGURE 5.9 (a) Histochemical staining for fiber type after a 30 km run; a type II (fast-twitch) fiber is
circled. (b) Histochemical staining for muscle glycogen after the run. Note that a number of type II
fibers still have glycogen, as noted by their darker stain, whereas most of the type I (slow-twitch) fibers
are depleted of glycogen.
The pattern of glycogen depletion from type I and type II fibers
depends on the exercise intensity. Recall that type I fibers are the
first fibers to be recruited during light exercise. As muscle tension
requirements increase, type IIa fibers are added to the workforce. In
exercise approaching maximal intensities, the type IIx fibers are
added to the pool of recruited fibers.
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FIGURE 5.10 Muscle glycogen use in the vastus lateralis, gastrocnemius, and soleus muscles during
2 h of level, uphill, and downhill running on a treadmill at 70% of O2max. Note that the greatest
glycogen use is in the gastrocnemius during uphill and downhill running.
In addition to selectively depleting
glycogen from type I or type II fibers, exercise may place unusually
heavy demands on select muscle groups. In one study, subjects ran
on a treadmill positioned for uphill, downhill, and level running for 2 h
Depletion in Different Muscle Groups
318
at 70% of O2max. Figure 5.10 compares the resultant glycogen
depletion in three muscles of the lower extremity: the vastus lateralis
(knee extensor), the gastrocnemius (ankle extensor), and the soleus
(another ankle extensor).
The results show that whether one runs uphill, downhill, or on a
level surface, the gastrocnemius uses more glycogen than does the
vastus lateralis or the soleus. This suggests that the ankle extensor
muscles are more likely to become depleted during distance running
than are the thigh muscles, isolating the site of fatigue to the lower
leg muscles.
Muscle glycogen alone cannot
provide enough carbohydrate for exercise lasting several hours.
Glucose delivered by the blood to the muscles contributes a lot of
energy during endurance exercise. The liver breaks down its stored
glycogen to provide a constant supply of blood glucose. In the early
stages of exercise, energy production requires relatively little blood
glucose, but in the later stages of an endurance event, blood glucose
may make a large contribution. To keep pace with the muscles’
glucose uptake, the liver must break down increasingly more
glycogen as exercise duration increases.
Liver glycogen stores are limited, and the liver cannot produce
glucose rapidly from other substrates. Consequently, blood glucose
concentration can decrease when muscle uptake exceeds the liver’s
glucose output. Unable to obtain sufficient glucose from the blood,
the muscles must rely more heavily on their glycogen reserves,
accelerating muscle glycogen depletion and leading to earlier
exhaustion.
Not surprisingly, endurance performances improve when the
muscle glycogen supply is elevated before the start of activity. On
the other hand, most studies have shown no effect of carbohydrate
ingestion on net muscle glycogen utilization during prolonged,
strenuous exercise. The importance of muscle glycogen storage for
endurance performance is discussed in chapter 15. For now, note
that glycogen depletion and hypoglycemia (low blood sugar) limit
performance in activities lasting longer than 60 min.
Glycogen Depletion and Blood Glucose
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It does not appear likely
that glycogen depletion directly causes fatigue during endurance
exercise performance, but it may play an indirect role. We cannot
explain precisely why muscle function is impaired when muscle
glycogen is low, but this is usually explained by a compromised rate
of ATP production. Glycogen is more than simply a form for
carbohydrate storage; it also acts as a regulator of several cellular
functions. To aid in that role, glycogen is not distributed
homogeneously throughout the muscle fiber but localized in distinct
pools. Evidence suggests that depletion of glycogen granules
localized within the myofibrils interferes with excitation–contraction
coupling and Ca2+ release from the sarcoplasmic reticulum.20
Mechanisms of Fatigue with Glycogen Depletion
Metabolic By-Products and Fatigue
Various by-products of metabolism have been implicated as factors
causing, or contributing to, fatigue. The metabolic by-products that
have received the most attention in discussions of fatigue are
inorganic phosphate, heat, lactate, and hydrogen ions.
Inorganic Phosphate
Inorganic phosphate increases during intense short-term exercise as
PCr and ATP are being broken down. It now appears that Pi, which
accumulates during intense short-term exercise from the breakdown
of ATP, may be the largest contributor to fatigue in this type of
exercise.26 Excess Pi directly impairs contractile function of the
myofibrils and can reduce Ca2+ release from the sarcoplasmic
reticulum. Increases in both Pi and ADP also inhibit ATP breakdown
through negative feedback.
Heat and Muscle Temperature
Recall that energy expenditure results in a relatively large heat
production, some of which is retained in the body, causing core
temperature to rise. Exercise in the heat can increase the rate of
carbohydrate utilization and hasten glycogen depletion, effects that
may be stimulated by the increased secretion of epinephrine. It is
hypothesized that high muscle temperatures impair both skeletal
muscle function and muscle metabolism.
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The ability to continue moderate- to high-intensity cycle
performance is affected by ambient temperature. Galloway and
Maughan12 studied performance time to exhaustion of male cyclists
at four different air temperatures: 4 °C (38 °F), 11 °C (51 °F), 21 °C
(70 °F), and 31 °C (87 °F). Results of that study are shown in figure
5.11. Time to exhaustion was longest when subjects exercised at an
air temperature of 11 °C and was shorter at colder and warmer
temperatures. Fatigue set in earliest at 31 °C. Similarly, at a given
warm air temperature, increasing relative humidity caused early
fatigue.16 Precooling of muscles similarly prolongs exercise, while
preheating causes earlier fatigue. Heat acclimation, discussed in
chapter 12, spares glycogen and reduces lactate accumulation.
Lactic Acid
Recall that lactic acid is a by-product of anaerobic glycolysis.
Although most lay people believe that lactic acid is responsible for
fatigue in all types of exercise, lactic acid undergoes constant
turnover and, as described in chapter 2, is recycled to provide
energy. Lactic acid produced within the cytoplasm of a muscle fiber
can be taken up by mitochondria within that same muscle fiber and
oxidized for ATP formation. Lactic acid can also be shuttled to other
sites where it can be oxidized. In fact, lactic acid only accumulates
within a muscle fiber during relatively brief, highly intense muscular
effort. Marathon runners often have near-baseline lactic acid
concentrations at the end of the race, despite notable fatigue. As
noted in the previous section, their fatigue is likely caused by
inadequate energy supply, not excess lactic acid.
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FIGURE 5.11 Time to exhaustion for a group of men performing cycle exercise at about 70%
O2max.
(a) The subjects were able to perform longer (delay fatigue longer) in a cool environment of 11 °C.
Exercising in colder or warmer conditions hastened fatigue. (b) At an ambient temperature of 30 °C,
increased relative humidity decreased time to exhaustion.
(a) Adapted by permission from S.D.R. Galloway and R.J. Maughan, “Effects of Ambient Temperature on the
Capacity to Perform Prolonged Cycle Exercise in Man,” Medicine and Science in Sports and Exercise 29 (1997):
1240-1249. (b) Reprinted by permission from R.J. Maughan et al., “Influence of Relative Humidity on Prolonged
Exercise Capacity in a Warm Environment,” European Journal of Applied Physiology 112 (2012): 2313-2321.
Short sprints in running, cycling, and swimming can all lead to
large accumulations of lactic acid. While the presence of lactic acid
in itself cannot be blamed for the feeling of fatigue, if it is not cleared,
the lactic acid dissociates, converting to lactate and causing an
accumulation of hydrogen ions.
Hydrogen Ions
While the lactate ion does not appear to have any major negative
effects on the ability to generate force, H+ accumulation causes
muscle acidosis (decreased pH).
Activities of short duration and high intensity, such as sprint
running and sprint swimming, depend heavily on anaerobic
glycolysis and produce large amounts of lactate and H+ within the
muscles. Fortunately, the cells and body fluids possess buffers, such
as bicarbonate (HCO3−), that minimize the disrupting influence of the
H+. Without these buffers, H+ would lower the pH to about 1.5, killing
the cells. Because of the body’s buffering capacity, the H+
concentration remains low even during the most severe exercise,
allowing muscle pH to decrease from a resting value of 7.1 to no
lower than 6.4 at exhaustion after high-intensity activity.
However, pH changes of this magnitude can adversely affect
energy production and muscle contraction. An intracellular pH below
6.9 inhibits the action of phosphofructokinase, an important glycolytic
enzyme, slowing the rate of glycolysis and ATP production. At a pH
of 6.4, the influence of H+ stops any further glycogen breakdown,
causing a rapid decrease in ATP and ultimately exhaustion. In
addition, H+ may lower the amount of calcium released from the
sarcoplasmic reticulum, interfering with the coupling of the actin–
myosin cross-bridges and decreasing the muscle’s contractile force.
However, the impact on muscle force production is small. A larger
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impact comes from H+ acting to decrease the myofilaments’
sensitivity to calcium, causing a loss of contractile force and
velocity.8 Because of those effects, low muscle pH may be a primary
cause of fatigue during maximal, all-out exercise lasting 20 to 30 s.
As seen in figure 5.12, reestablishing the preexercise muscle pH
after an exhaustive sprint bout requires about 30 to 35 min of
recovery. Even when normal pH is restored, blood and muscle
lactate levels can remain quite elevated. However, experience has
shown that an athlete can continue to exercise at relatively high
intensities even with a muscle pH below 7.0 and a blood lactate level
above 6 or 7 mmol/L, four to five times the resting value.
FIGURE 5.12 Changes in muscle pH during sprint exercise and recovery. Note the drastic decrease in
muscle pH during the sprint and the gradual recovery to normal after the effort. Note that it took more
than 30 min for pH to return to its preexercise level.
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Neuromuscular Fatigue
Thus far we have considered only factors within the muscle that
might be responsible for fatigue. Evidence also suggests that under
some circumstances, fatigue may result from an inability to activate
the muscle fibers, a function of the nervous system. As noted in
chapter 3, the nerve impulse is transmitted across the
neuromuscular junction to activate the fiber’s membrane, and it
causes the fiber’s sarcoplasmic reticulum to release calcium. The
calcium, in turn, binds with troponin to initiate muscle contraction, a
process collectively called excitation–contraction coupling. Several
possible neural mechanisms could disrupt this process and possibly
contribute to fatigue, and two of those—one peripheral and one
central—are discussed next.
Neural Transmission
Fatigue may occur at the neuromuscular junction, preventing nerve
impulse transmission to the muscle fiber membrane. Studies in the
early 1900s clearly established such a failure of nerve impulse
transmission in fatigued muscle. This failure may involve one or
more of the following processes:
The release or synthesis of acetylcholine (ACh), the
neurotransmitter that relays the nerve impulse from the motor
nerve to the muscle membrane, might be reduced.
Cholinesterase, the enzyme that breaks down ACh once it
has relayed the impulse, might become hyperactive,
preventing sufficient concentration of ACh to initiate an action
potential.
Cholinesterase activity might become hypoactive (inhibited),
allowing ACh to accumulate excessively, inhibiting relaxation.
The muscle fiber membrane might develop a higher
threshold for stimulation by motor neurons.
Some substance might compete with ACh for the receptors
on the muscle membrane without activating the membrane.
Potassium might leave the intracellular space of the
contracting muscle, decreasing the membrane potential to
half of its resting value.
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Although most of these causes for a neuromuscular block have been
associated with neuromuscular diseases (such as myasthenia
gravis), they may also cause some forms of neuromuscular fatigue.
Some evidence suggests that fatigue also may be attributable to
calcium retention within the sarcoplasmic reticulum, which would
decrease the calcium available for muscle contraction. In fact,
depletion of PCr and lactate buildup might simply increase the rate of
calcium accumulation within the sarcoplasmic reticulum. However,
these theories of fatigue remain speculative.
Central Nervous System
The discussion to this point suggests that fatigue is due to peripheral
changes that limit or completely stop further effective muscular
actions. The recruitment of muscle depends, in part, on conscious or
subconscious control by the brain. An alternate theory to peripheral
fatigue, termed the central governor theory, proposes that
processes occur in the brain that regulate power output by the
muscles to maintain homeostasis and prevent unsafe levels of
exertion that may damage tissues or cause catastrophic events. The
central governor limits exercise by decreasing the recruitment of
muscle fibers, which in turn causes fatigue. While this theory has
been hotly debated in recent years, the concept of a central
“governor” was first proposed by A.V. Hill (see introductory chapter)
in 1924.
In a 2012 study, researchers in Switzerland sought to separate out
the central and peripheral contributors to muscle fatigue during lowintensity isometric contraction of the knee extensor muscles using an
innovative protocol.18 Subjects performed a sustained isometric
muscle contraction at 20% of the maximal voluntary contraction
(MVC) until they experienced fatigue, defined as the point at which
they could no longer maintain the 20% MVC force output. Then, the
muscle was immediately electrically stimulated to maintain the same
force output for 1 min, followed by an immediate voluntary effort to
maintain that same force once again. In essence, fatigue was
induced, and then the external electrical stimulation took over for the
brain and the motor neuron to continue to produce force. If the initial
fatigue was caused by problems with excitation–contraction coupling
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(peripheral factors), then electrically stimulated muscle would still be
fatigued and not able to produce force. Conversely, if fatigue was
due to problems with the motor neuron or central neural factors,
electrical stimulation would cause the muscle to generate force once
again. The researchers also measured the maximal amount of force
that could be voluntarily generated before and after fatigue was
induced.
RESEARCH PERSPECTIVE 5.2
Can You Talk Yourself Out of Fatiguing?
As endurance sports become increasingly popular, the number of people
participating in competitive endurance events is growing. Successful
performance in endurance events requires the ability to sustain aerobic
exercise over an extended period of time (that is, to delay the onset of fatigue
as long as possible), and performance-enhancing strategies to increase the
intensity and duration of the activity are important for athletes in these sports.
Because fatigue defines the upper limit of endurance, research efforts have
targeted understanding the physiological and psychological causes of fatigue
and how to delay their effects.
During long-duration endurance events such as marathons or triathlons,
many exercise physiologists believe that fatigue is the result of depleting
energy stores within the body, and the physiological causes of fatigue are
discussed in detail in this chapter. Alternatively, the psychobiological model of
endurance performance suggests that fatigue is caused by the conscious
decision to terminate a given activity, rather than by physiological limits.
According to this model, the ultimate determinant of endurance performance
in highly motivated athletes is the conscious perception of how hard, heavy,
and strenuous the effort is. Based on this reasoning, strategies to reduce the
perception of effort may delay the onset of fatigue in endurance athletes.
One strategy that may reduce fatigue according to the psychobiological
model of endurance performance is self-talk, or self-addressed
verbalizations, either aloud or silently. Self-talk can be both instructional and
motivational for athletes, and it has been suggested to improve performance
on effort-based tasks by motivating athletes to push themselves further even
when the perceptual drive to terminate exercise is high. A 2014 study of 24
recreationally active men and women investigated the effect of self-talk on
endurance performance during high-intensity cycling exercise.3 After baseline
data were recorded, research subjects were divided into two groups: One
group received 2 weeks of coaching and practice in the use of self-talk while
the other group (control group) did not. After the 2 weeks, all of the
participants returned to the laboratory for retesting, and their performance
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results were compared to those from the beginning of the study. The group of
subjects who received the self-talk coaching had a lower rating of perceived
exertion (RPE) and a longer time to exhaustion (by almost 2 min) compared
to their first visit (see figure); however, the results for the control group did not
change. Motivational self-talk can reduce the perceived effort and increase
endurance performance during aerobic activity. Training with psychobiological
interventions that reduce the perception of effort may improve endurance
performance in endurance athletes by delaying fatigue.
Changes in time to exhaustion after 2 weeks in the control group (dotted line) and the
group of subjects who received 2 weeks of self-talk training (solid line). The self-talk
group showed improvements in endurance after the self-talk training, while the
control group did not change across the 2 weeks.
They found that when the electrical stimulation was applied after
fatigue, the muscle was again able to maintain 20% MVC, indicating
that, given the proper neural stimulation, the muscle itself maintains
the ability to contract and generate force. When they recorded the
muscle’s electrical activity during the MVC after fatigue, they found
that muscle activation by the nervous system increased greatly,
suggesting that the reduced force of the maximal contraction was
due to impairments of the contractile elements. Overall, this study
suggests that the initial fatigue experienced after a bout of
submaximal exercise is likely due to a reduction in central neural
factors, whereas the impairments in maximal contraction are due to
peripheral factors related to changes in excitation–contraction
coupling.
Undoubtedly, there is some central nervous system (CNS)
involvement in most types of fatigue. When a subject’s muscles
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appear to be nearly exhausted, verbal encouragement, shouting,
music, or even direct electrical stimulation of the muscle can
increase the strength of muscle contraction. The precise
mechanisms underlying the CNS role in causing, sensing, and even
overriding fatigue are not fully understood. Unless they are highly
motivated, most individuals terminate exercise before their muscles
are physiologically exhausted. To achieve peak performance,
athletes train to learn proper pacing and tolerance for fatigue.
Other Contributors to Fatigue
As one can appreciate from the previous sections, the underlying
causes of fatigue are many and varied and depend largely on the
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intensity and duration of the exercise being performed. Recent
research has also uncovered roles for impaired mitochondrial
function and reactive oxygen species in some types of fatigue. A
group of French investigators reported that impaired mitochondrial
function led to both a slower rate of PCr recovery and a reduction in
oxidative ATP production after dynamic submaximal exercise.10
However, the extent to which those effects can be attributed to
cellular acidosis or muscle damage is unclear.
Michael Reid provided a compelling case that reactive oxygen
species (ROS) accumulation in working muscle contributes to the
loss of function that occurs in muscle fatigue.25 These molecules,
including hydrogen peroxide, superoxide, and hydroxyl radicals,
increase during strenuous muscle contractions. They are present in
myofibrillar cytoplasm and organelles, in interstitial fluid, and within
the vascular space. Two lines of evidence point to a role for these
chemically reactive molecules: (1) Directly exposing muscle cells to
ROS evokes many of the same changes that occur with fatigue
during exercise and (2) pretreating the muscle with antioxidants
delays fatigue.
In Review
Depending on the circumstances, fatigue may result from depletion of PCr or
glycogen; both situations impair ATP production. Glycogen depletion may occur
in select fiber types or specific muscle groups depending on the exercise.
Increased metabolic by-products like phosphate ions and heat may contribute to
fatigue.
Lactic acid often has been blamed for fatigue, but it is generally not directly
related to fatigue during prolonged endurance exercise, and may serve as a fuel
source (see chapter 2).
In short-duration exercise, like sprinting, the H+ generated by dissociation of
lactic acid may contributes to fatigue. The accumulation of H+ decreases muscle
pH, which impairs the cellular processes that produce energy and muscle
contraction.
Failure of neural transmission may be a cause of some types of fatigue. Many
mechanisms can lead to such failure, and further research is needed.
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The CNS plays a role in most types of fatigue, perhaps limiting exercise
performance as a protective mechanism. Perceived fatigue usually precedes
physiological fatigue, and athletes who feel exhausted can often be encouraged
to continue by various cues that stimulate the CNS, such as music or self-talk.
Critical Power: The Link Between Energy
Expenditure and Fatigue
An athlete who can sustain a high level of exercise intensity for a
prolonged period without fatiguing will be successful. Exercise
physiologists have a name for the link between optimal performance
and fatigue: critical power. The critical power defines the tolerable
duration of high-intensity exercise. If we graph the relation between
power output (or exercise intensity, or speed) and the maximal time
that intensity can be maintained, the line is curvilinear, as depicted in
figure 5.13. At very high power outputs, exercise can be performed
only for short durations. But as intensity is progressively decreased,
exercise can be performed for longer and longer durations. At some
point, this relation levels off and reaches an asymptote, defining the
critical power for that activity—the maximal intensity that can be
sustained without fatigue limiting performance.
Critical power represents the highest metabolic rate that is
maintained entirely by oxidative metabolism. In that regard, it is
related to the lactate threshold (discussed earlier in this chapter), but
occurs at slightly higher intensities. Not surprisingly, critical power is
increased with endurance or high-intensity interval training and
decreased with aging and in chronic disease states. Hypoxia, such
as that encountered at altitude (discussed in chapter 13), also
reduces critical power, while breathing elevated oxygen
concentrations elevates it.
Critical power is a useful measure in sport and exercise
physiology because it correlates well with performance in running,
rowing, swimming, and even team sport activities lasting from a few
min to 2 h.28 However, while exercise at or below the critical power
should theoretically be able to be continued indefinitely, in reality
exercise at the critical power cannot be sustained beyond 30 min or
so. With much attention being paid to breaking the 2 h barrier for the
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marathon, the critical power concept would dictate that a runner has
to sustain a critical speed of only 21.1 km/h (13.1 mph, or slightly
under 4.6 min miles); however, sustaining that heavy-intensity pace
for 2 h has proven virtually impossible.28
FIGURE 5.13 The relation between power output (in watts [W]) and the time that power output can be
maintained. The critical power is defined as the asymptote in the relation, i.e., the maximal power
output that can be sustained without fatigue limiting the duration of performance.
Muscle Soreness and Muscle Cramps
Muscle soreness generally results from exercise that is exhaustive or
of very high intensity. This is particularly true when people perform a
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specific exercise for the first time. While muscle soreness can be felt
at any time, there is generally a period of mild muscle soreness that
can be felt during and immediately after exercise and then a more
intense soreness felt a day or two later.
Acute Muscle Soreness
Pain felt during and immediately after exercise is classified as a
muscle strain and is perceived as muscle stiffness, aching, or
tenderness. It can result from accumulation of the end products of
exercise, such as H+, and from tissue edema that is caused by fluid
shifting from the blood plasma into the tissues. Edema is the cause
of the acute muscle swelling that people feel after heavy endurance
or strength training. The pain and soreness usually disappear within
several hours after the exercise. Thus, this soreness is often referred
to as acute muscle soreness.
Delayed-Onset Muscle Soreness
The precise causes of muscle soreness felt a day or two after a
heavy bout of exercise are not totally understood. Because this pain
does not occur immediately, it is referred to as delayed-onset
muscle soreness (DOMS). Delayed-onset muscle soreness can
vary from slight muscle stiffness to severe, debilitating pain that
restricts movement. In the following sections, we discuss some
theories that attempt to explain this form of muscle soreness.
RESEARCH PERSPECTIVE 5.3
Are Muscle Fatigue and Exercise Inefficiency the Same
Thing?
During whole-body exercise, fatigue and decreased efficiency (the ratio of
mechanical energy output, or external work performed, to metabolic energy
production) are major causes of exercise intolerance and resulting early
termination of an acute exercise bout. Exercise physiologists agree that these
two concepts, fatigue and decreased efficiency, contribute to exercise
intolerance, but are they linked?
Decreased efficiency typically precedes exercise termination during highintensity exercise. There is an increased oxygen cost of work during constant
power output and incremental exercise above the lactate threshold. This is
most clearly seen with O2 drift during steady-state exercise, where O2
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slowly increases despite a constant power output; this increased oxygen cost
for the same amount of work is evidence of a decreased efficiency of muscle
contraction. Similarly, during incremental exercise, O2 increases in excess
of predicted need for power outputs above the lactate threshold. In fact,
during incremental exercise, efficiency is reduced by approximately 20% for
power outputs above the lactate threshold. As a consequence of this
inefficiency, the exerciser reaches his or her peak O2 at a lower power
output, resulting in muscle fatigue and ultimately failure to continue. Overall,
the decline in skeletal muscle efficiency during high-intensity exercise above
the lactate threshold dictates a greater oxygen demand to produce the same
mechanical power, termed inefficiency. Because the energy produced by the
muscle is limited, the rate at which this inefficiency develops is a major
determinant of fatigue and task failure.
But what is causing muscle inefficiency at high power outputs? The fact
that muscle fatigue during whole-body exercise occurs only at intensities
above the lactate threshold (where ATP production relies on contributions
from substrate-level phosphorylation) may provide clues, and the factors
affecting the ratio between ATP resynthesis and oxygen consumption by the
muscle mitochondria may provide the answer. A 2014 study using combined
magnetic resonance spectroscopy and pulmonary gas exchange in humans
found that the tight relation between ATP production and
O2 that is
observed at moderate-intensity exercise was lost at exercise intensities
above the lactate threshold.5 This finding suggests that muscle inefficiency is
due to impairments in ATP production and turnover.
As discussed in this chapter, many intracellular mechanisms, including
changes in oxygen and substrate availability, impaired function of the
ATPases, decreased pH, increased temperature, altered Na+/K+ pump
function, and changes in motor unit recruitment patterns have all been
studied and shown to contribute to reduced muscle efficiency and muscle
fatigue. Impairments in ATP turnover and production challenge the cellular
homeostasis of the muscle fiber. In this scenario, muscle fatigue may be a
protective mechanism that prevents muscle fiber damage. Changes in
muscle cellular processes during high-intensity aerobic exercise provide a
link between this inefficiency and muscle fatigue that ultimately leads to
failure.13 However, no one has shown a clear cause–effect relation between
muscle fatigue and decreased efficiency. Future research is necessary to tell
if fatigue and inefficiency are in fact the same thing.
Almost all current theories acknowledge that eccentric muscle
action is the primary initiator of DOMS. This has been clearly
demonstrated in a number of studies examining the relationship of
muscle soreness to eccentric, concentric, and static actions.
333
Individuals who train solely with eccentric actions experience
extreme muscle soreness, whereas those who train using only static
and concentric actions experience little soreness. This idea has been
further explored in studies in which subjects ran on a treadmill for 45
min on two separate days, one day on a level grade and the other
day on a 10% downhill grade.26,27 No muscle soreness was
associated with the level running. But the downhill running, which
required extensive eccentric action, resulted in considerable
soreness within 24 to 48 h, even though blood lactate
concentrations, previously thought to cause muscle soreness, were
much higher with level running.
In the following sections we examine some of the proposed
explanations for exercise-induced DOMS. In general, the pathway
for developing DOMS begins with structural damage to muscle fibers
(microtrauma) and to the surrounding connective tissues. This
damage is followed by an inflammatory process that leads to edema
as fluid and electrolytes shift into the area. To make matters worse,
muscle spasms can occur, prolonging the condition and making the
soreness worse.
Structural Damage
The presence of increased concentrations of several specific muscle
enzymes in blood after intense exercise suggests that some
structural damage may occur in the muscle membranes. These
enzyme concentrations in the blood increase from 2 to 10 times
following bouts of heavy training. Recent studies support the idea
that these changes might indicate various degrees of muscle tissue
breakdown. Examination of tissue from the leg muscles of marathon
runners has revealed remarkable damage to the muscle fibers after
both training and marathon competition. The onset and timing of
these muscle changes parallel the degree of muscle soreness
experienced by the runners.
Figure 5.14 shows changes in the contractile filaments and Zdisks before and after a marathon race. Recall that Z-disks are the
points of contact for the contractile proteins. They provide structural
support for the transmission of force when the muscle fibers are
activated to shorten. Figure 5.14b, after the marathon, shows
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moderate Z-disk streaming and major disruption of the thick and thin
filaments in a parallel group of sarcomeres as a result of the force of
eccentric actions or stretching of the tightened muscle fibers.
Although the effects of muscle damage on performance are not
fully understood, it is generally agreed that this damage is
responsible in part for the localized muscle pain, tenderness, and
swelling associated with DOMS. However, blood enzyme
concentrations might increase and muscle fibers might be damaged
frequently during daily exercise that produces no muscle soreness.
Also, remember that muscle damage appears to be a precipitating
factor for muscle hypertrophy.
FIGURE 5.14 (a) An electron micrograph showing the normal arrangement of the actin and myosin
filaments and Z-disk configuration in the muscle of a runner before a marathon race. (b) A muscle
sample taken immediately after a marathon race shows moderate Z-disk streaming and major
disruption of the thick and thin filaments in a parallel group of sarcomeres, caused by the eccentric
actions of running.
Reprinted by permission from S.M. Roth et al., “High-Volume, Heavy-Resistance Strength Training and Muscle
Damage in Young and Older Women,” Journal of Applied Physiology 88 (2000): 1112-1118. Image courtesy of Dr.
Roth.
Inflammatory Reaction
White blood cells serve as a defense against foreign materials that
enter the body and against conditions that threaten the normal
function of tissues. The white blood cell count tends to increase
following activities that induce muscle soreness, leading some
investigators to suggest that soreness results from inflammatory
reactions in the muscle. But the link between these reactions and
muscle soreness has been difficult to establish.
335
In early studies, researchers attempted to use drugs to block the
inflammatory reaction, but these efforts were unsuccessful in
reducing either the amount of muscle soreness or the degree of
inflammation. These early results did not support a link between
simple inflammatory mediators and DOMS. However, more recent
studies have begun to establish a link between muscle soreness and
inflammation. It is now recognized that substances released from
injured muscle can act as attractants, initiating the inflammatory
process. Mononucleated cells in muscle are activated by the injury,
providing the chemical signal to circulating inflammatory cells.
Neutrophils (a type of white blood cell) invade the injury site and
release cytokines (immunoregulatory substances), which then attract
and activate additional inflammatory cells. Neutrophils possibly also
release oxygen free radicals that can damage cell membranes. The
invasion of these inflammatory cells is also associated with the
incidence of pain, thought to be caused by a release of substances
from the inflammatory cells stimulating the pain-sensitive nerve
endings. Macrophages (another type of cell of the immune system)
then invade the damaged muscle fibers, removing debris through a
process known as phagocytosis. Last, a second phase of
macrophage invasion occurs, which is associated with muscle
regeneration.
Sequence of Events in DOMS
The general consensus among researchers is that a single theory or
hypothesis cannot explain the mechanism causing DOMS. Instead
researchers have proposed a sequence of events that may explain
the DOMS phenomenon, including the following:
1. High tension in the contractile-elastic system of muscle results
in structural damage to the muscle and its cell membrane.
This is also accompanied by excessive strain of the
connective tissue.
2. The cell membrane damage disturbs calcium homeostasis in
the injured fiber, inhibiting cellular respiration. The resulting
high calcium concentrations activate enzymes that degrade
the Z-lines.
336
3. Within a few hours there is a significant elevation in circulating
neutrophils that participate in the inflammatory response.
4. The products of macrophage activity and intracellular contents
(such as histamine, kinins, and K+) accumulate outside the
cells. These substances then stimulate the free nerve endings
in the muscle. This process appears to be accentuated in
eccentric exercise, in which large forces are distributed over
relatively small cross-sectional areas of the muscle.
5. Fluid and electrolytes shift into the area, creating edema,
which causes tissue swelling and activates pain receptors.
Muscle spasms may also be present.
DOMS and Performance
With DOMS comes a reduction in the force-generating capacity of
the affected muscles. Whether the DOMS is the result of injury to the
muscle or edema, the affected muscles are not able to exert as
much force when the person is asked to apply maximal force, as in
the performance of a 1-repetition maximum strength test. Maximal
force-generating capacity gradually returns over days or weeks. The
loss of strength is the result of
1. the physical disruption of the muscle as illustrated in figure
5.14,
2. failure within the excitation–contraction coupling process, and
3. loss of contractile protein.
Failure in excitation–contraction coupling appears to be the most
important, particularly during the first 5 days. This is illustrated in
figure 5.15.
Muscle glycogen resynthesis also is impaired when a muscle is
damaged. Resynthesis is generally normal for the first 6 to 12 h after
exercise, but it slows or stops completely as the muscle undergoes
repair, thus limiting the fuel storage capacity of the injured muscle.
Figure 5.16 illustrates the time sequence of the various markers of
muscle damage associated with intense eccentric exercise of the
elbow flexor muscles as compared to concentric exercise. As shown
in the figure, changes in function (MVC and range of motion), muscle
swelling (circumference), soreness, and molecular indicators of
337
damage (creatine kinase activity and myoglobin concentration)
persist for several days.
Minimizing DOMS
Reducing the negative effects of DOMS is important for maximizing
training gains. The eccentric component of muscle action could be
minimized during early training, but this is not possible for athletes in
most sports. An alternative approach is to start training at a very low
intensity and progress slowly through the first few weeks. Yet
another approach is to initiate the training program with a highintensity, exhaustive training bout. Muscle soreness would be great
for the first few days, but evidence suggests that subsequent training
bouts would cause considerably less muscle soreness. Because the
factors associated with DOMS are also potentially important in
stimulating muscle hypertrophy, DOMS is most likely necessary to
maximize the training response.
338
FIGURE 5.15 Estimated contributions of excitation–contraction (EC) coupling failure, decreased
contractile protein content, and physical disruption to the decrease in strength following muscle injury.
Reprinted by permission from G. Warren et al., “Excitation-Contraction Uncoupling: Major Role in ContractionInduced Muscle Injury,” Exercise and Sport Sciences Reviews 29, no. 2 (2001): 82-87
Statins and Skeletal Muscle Soreness
3-Hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, or
statins, are the most commonly prescribed cardiovascular drugs in
the world. Statins are extremely effective at reducing serum
cholesterol concentration and reducing the risk of future
cardiovascular events. The most common side effect associated with
taking statins is muscle pain, which is reported to occur in up to 25%
of patients.23 Muscle pain from statins can range from mild soreness
including cramps and weakness to a life-threatening condition
associated with a severe breakdown of muscle tissue called
rhabdomyolysis. While the precise mechanism for how statins may
contribute to muscle soreness and damage is unclear, it has been
linked to excessive production of reactive oxygen molecules by the
mitochondria and changes in the way muscle cells get rid of
damaged proteins.
FIGURE 5.16 The responses of various physiological markers of muscle damage after eccentric and
concentric exercise by elbow flexors. The changes persist for several days and include (a) MVC and
(b) range of motion (ROM), both indicators of muscle function; (c) muscle swelling (circumference); (d)
creatine kinase (CK) and (e) plasma myoglobin (Mb) concentration, both molecular indicators of
damage; and (f) soreness.
339
Reprinted by permission from K. Nosaka, Muscle Soreness and Damage and the Repeated-Bout Effect, in Skeletal
Muscle Damage and Repair, edited by Peter Tiidus (Champaign, IL: Human Kinetics, 2008). Data from A.P.
Lavender and K. Nosaka, “Changes in Steadiness of Isometric Force Following Eccentric and Concentric
Exercise,” European Journal of Applied Physiology 96 (2006): 235-240.
Statin use increases creatine kinase concentration after eccentric
exercise, a clinical marker of muscle protein breakdown. However,
patients who take statins may have muscle pain without an increase
in creatine kinase, suggesting that other mechanisms might be
causing pain.22 While trained individuals may be able to tolerate pain
during vigorous exercise, in some people, statin-associated muscle
pain may limit even leisure-type physical activity.4 Additionally, recent
exercise training studies in older people indicate that statin users do
not fully adapt to the training stimulus.17 Because exercise is a
cornerstone therapy for treating and preventing cardiovascular
disease, much more research needs to be done to more fully
understand the effects of statins on skeletal muscle physiology and
how to optimize the beneficial effects of both therapies.
In Review
Acute muscle soreness occurs during or immediately after an exercise bout.
Delayed-onset muscle soreness usually peaks a day or two after the exercise
bout. Eccentric muscle action seems to be the primary initiator of this type of
soreness.
Proposed causes of DOMS include structural damage to muscle cells and
inflammatory reactions within the muscles. The proposed sequence of events
includes structural damage, impaired calcium homeostasis, inflammatory
response, increased macrophage activity, and edema.
Reduced muscle strength with DOMS is likely the result of physical disruption of
the muscle, failure of the excitation–contraction process, and loss of contractile
protein.
Muscle soreness can be minimized through the use of lower intensity and fewer
eccentric contractions early in training. However, muscle soreness may ultimately
be an important part of maximizing the resistance training response.
RESEARCH PERSPECTIVE 5.4
340
Delayed-Onset Muscle Soreness May Be Different in
Men and Women
Creatine kinase is the enzyme that catalyzes the exchange of high-energy
phosphate bonds between phosphocreatine and ADP to supply ATP to the
working muscle during exercise. When creatine kinase appears in the blood,
it can indicate metabolic and mechanical disturbances in the muscle cell.
Following eccentric exercise in men, creatine kinase activity measured in the
blood correlates with muscle soreness and decrements in maximal isometric
strength. Men have higher blood creatine kinase activity compared to women,
which may be due to the actions of circulating estrogens. The creatine kinase
response to exercise may be lower when women are tested during periods of
higher circulating estrogen concentration (e.g., the late follicular phase
preceding ovulation) compared to periods of low circulating estrogen. Some
studies of sex differences in reported muscle soreness suggest that women
have a reduced perception of soreness following eccentric exercise
compared to men, but other studies have found no differences. Interestingly,
the creatine kinase response to exercise is correlated with delayed-onset
muscle soreness (DOMS) in men but not in women. Altogether, there is still
debate about whether sex differences in the creatine kinase response to
exercise, and in DOMS, exist in humans.
A recent study conducted in South Africa set out to determine whether the
serum creatine kinase response and the perception of DOMS following a
bout of downhill running were influenced by sex and if the magnitudes of
those responses depended on the circulating estrogen concentrations in the
women.19 In that study, 21 sedentary subjects (6 men and 15 women)
performed 20 min of downhill running on a treadmill in the laboratory. Blood
samples were collected before exercise, immediately after exercise, and then
24, 48, and 72 h after exercise. Blood samples were analyzed for creatine
kinase activity and for estrogen and progesterone concentrations in the
women. The researchers also assessed DOMS at the same time points by
having the subjects rate their perception of soreness when standing from a
seated position on a visual scale from “no pain” to “the worst pain ever
experienced.”
The 24 h peak creatine kinase response to this bout of downhill running
was the same between men and women; however, circulating creatine kinase
activity was restored to preexercise baseline faster in women (by 48 h
postexercise) than in men (72 h after exercise). Neither estrogen nor
progesterone influenced the creatine kinase response in the women.
Interestingly, both men and women still reported muscle soreness at 72 h
after the eccentric exercise bout despite the recovery of creatine kinase in
women 24 h earlier. While feelings of muscle soreness were prolonged in
women who participated during the follicular phase of their menstrual cycle,
the researchers were not able to determine if the associated hormones
(estrogen or progesterone) were responsible for those findings.
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Overall, the study concluded that both creatine kinase and DOMS
responses to downhill running are affected by sex. Creatine kinase recovers
more quickly in women, regardless of circulating reproductive hormone
concentrations, but the recovery of muscle soreness is only correlated with
creatine kinase concentrations in men. While the DOMS response in women
may be affected by menstrual phase, a direct link to circulating hormones has
not been demonstrated.
Exercise-Induced Muscle Cramps
Skeletal muscle cramps are a frustrating problem in sport and
physical activity and commonly occur even in highly fit athletes.
Skeletal muscle cramps can come during the height of competition,
immediately after competition, or at night during deep sleep. Muscle
cramps are equally frustrating to scientists, because there are
multiple and unknown triggers and causes of muscle cramping, and
little is known about the best treatment and prevention strategies.
Nocturnal muscle cramps, especially in the calf muscle, have been
experienced by 60% of adults. This type of cramp is probably caused
by muscle fatigue and nerve dysfunction and may or may not be
associated with exercise. Electrolyte imbalances and hydration do
not seem to play an important role.
Exercise-associated muscle cramps (EAMCs), on the other
hand, are defined as painful, spasmodic, involuntary contractions of
skeletal muscles that occur during or immediately after exercise. Two
distinct theories have been proposed to explain the causes of
EAMCs, termed the neuromuscular control theory and the electrolyte
depletion theory.2
The neuromuscular control theory proposes that EAMCs occur
when some aspect of control between the motor neuron and the
muscle itself becomes altered. As muscle fatigue develops,
excitation of the muscle spindle and inhibition of the Golgi tendon
organ occur, resulting in abnormal α-motor neuron activity and
reduced inhibitory feedback. This abnormal firing of motor neurons
initially presents as muscle twitches or prefasciculations. If muscle
contraction continues, an EAMC occurs.
Risk factors associated with this type of cramping are age,
cramping history, and excessive exercise intensity and duration.
Several lines of evidence support this theory:
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1. This type of cramping is generally localized to the overworked
muscle.
2. Lack of conditioning, improper training, and depletion of
muscle energy stores, which are all associated with muscle
fatigue, can lead to the development of EAMCs.
3. Muscle cramping can be induced in the laboratory by
electrical stimulation or voluntary muscle contraction (with no
changes in electrolytes), which suggests that the mechanism
is neuromuscular in origin.
4. Often the most effective treatment for relieving cramps is
stretching of the muscle. Stretching increases tension in the
muscle and in the Golgi tendon organ that inhibits the α-motor
neuron.
5. Changing excitatory properties of the motor neuron—for
example, by ingesting transient receptor potential (TRP)
channel agonists—has been efficacious in attenuating both
electrically induced and voluntarily induced EAMCs.7
The second theory, electrolyte depletion, better describes a
different type of exercise-associated muscle cramp, often called heat
cramps. This type of muscle cramp typically occurs in athletes who
have been sweating extensively and have significant electrolyte
disturbances, mainly of sodium and chloride. These cramps involve
large muscle groups, and their occurrence is sometimes described
as “locking up.” This type of exertional heat cramp usually evolves
from small localized visible muscle fasciculations to severe and
debilitating muscle spasms. The cramps often begin in the legs but
can become widespread.
Because a significant amount of sodium can be lost only along
with a large loss of fluid, this theory is typically coupled with
dehydration. Progressive dehydration and electrolyte depletion
cause fluid to shift from the interstitial compartment to the
intravascular compartment. This contracts the extracellular fluid
compartment,
increasing
surrounding
neurotransmitter
concentrations and causing selected motor nerve terminals to
become hyperexcitable, leading to spontaneous discharge, initiation
of action potentials in the muscles, and ultimately EAMCs.
343
Proponents of this theory have espoused the following:
1. Anecdotal evidence has existed for centuries that laborers
working in hot and humid conditions suffered from cramping.
2. In those laborers, ingesting small volumes of salt water
prevented or alleviated the cramps.
3. Increases in sweat sodium concentration (“salty sweating”) is
evident in those athletes, specifically tennis and American
football players, who are most prone to cramping.9
VIDEO 5.1 Presents Mike Bergeron on the two types of muscle
cramping and the best ways to prevent muscle cramps.
Treatment of heat cramps involves the prompt ingestion of a highsalt solution (3 g in 500 ml of a sodium-containing beverage every 5
to 10 min) or intravenous fluid and sodium loading. In addition,
massage and ice application may help to calm the affected muscles
and relieve pain. Electrolyte-containing fluids should be continued if
dehydration and electrolyte loss are suspected.
To prevent EAMCs, the athlete should
be well conditioned, to reduce the likelihood of muscle
fatigue;
regularly stretch the muscle groups prone to EAMCs;
maintain fluid and electrolyte balance and carbohydrate
stores; and
reduce exercise intensity and duration if necessary.
344
In Review
Muscle fatigue-associated cramps are related to sustained α-motor neuron
activity, with increased muscle spindle activity and decreased Golgi tendon organ
activity.
Exercise-associated muscle cramps may be caused by altered neuromuscular
control, fluid or electrolyte imbalances, or both.
Heat-associated cramps, which typically occur in athletes who have been
sweating excessively, involve a shift in fluid from the interstitial space to the
intravascular space, resulting in a hyperexcitable neuromuscular junction.
Rest, passive stretching, holding the muscle in the stretched position, and fluid
and electrolyte restoration can be effective in treating EAMCs. Proper
conditioning, stretching, and nutrition are also possible prevention strategies.
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IN CLOSING
In previous chapters, we discussed how muscles and the nervous system
function together to produce movement. In this chapter we focused on energy
expenditure during exercise and fatigue. We considered the energy needed by
the body at rest and during movement. We explored how energy production
and availability can limit performance and learned that metabolic needs vary
considerably. We discussed the many potential factors involved in fatigue,
including those resulting from decreased energy delivery and accumulation of
metabolic by-products and those associated with the peripheral and central
nervous systems. We also introduced the concept of critical power as a link
between energy expenditure and fatigue. We also examined delayed-onset
muscle soreness and muscle cramps as additional limiting factors in exercise.
In the next chapter, we turn our attention to the cardiovascular system and its
control.
KEY TERMS
acute muscle soreness
basal metabolic rate (BMR)
calorie (cal)
calorimeter
cardiorespiratory endurance
central governor theory
critical power
delayed-onset muscle soreness (DOMS)
direct calorimetry
excess postexercise oxygen consumption (EPOC)
exercise-associated muscle cramps (EAMCs)
fatigue
Haldane transformation
indirect calorimetry
lactate threshold
maximal oxygen uptake ( O2max)
oxygen deficit
peak oxygen uptake ( O2peak)
respiratory exchange ratio (RER)
resting metabolic rate (RMR)
O2 drift
STUDY QUESTIONS
346
1.
Define direct calorimetry and indirect calorimetry, and describe how they
are used to measure energy expenditure.
2.
What is the respiratory exchange ratio (RER)? Explain why it is used to
determine the relative contributions of carbohydrate and fat to energy
expenditure.
3.
What are basal metabolic rate and resting metabolic rate, and how do they
differ?
4.
What is maximal oxygen uptake? How is it measured? What is its
relationship to sport performance?
5.
6.
Describe two possible markers of anaerobic capacity.
7.
What is economy of effort? How is it measured? What is its relationship to
sport performance?
8.
What is the relationship between oxygen consumption and energy
production?
9.
Why do athletes with high O2max values perform better in endurance
events than those with lower values?
10.
Why is oxygen consumption often expressed as milliliters of oxygen per
kilogram of body weight per minute (ml · kg−1 · min−1)?
11.
Describe the possible causes of fatigue during exercise bouts lasting 15 to
30 s and those lasting 2 to 4 h.
12.
Discuss three mechanisms through which lactate can be used as an
energy source.
13.
Define critical power and explain its usefulness in sport physiology. What is
its relation to sport performance?
14.
15.
What is the physiological basis for delayed-onset muscle soreness?
What is the lactate threshold? How is it measured? What is its relation to
sport performance?
What two theories have been proposed to explain the physiological basis
for exercise-associated muscle cramps? Provide support for each.
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter
QUIZ tests your understanding of the material covered in the chapter.
347
PART II
Cardiovascular and Respiratory
Function
In part I of this book, we learned how skeletal muscle contracts in
response to neural signaling and how the body produces energy
through metabolism to fuel its movement. We also examined
hormonal control of metabolism, of body fluid and electrolyte
balance, and of caloric intake. Finally, we looked at how energy
expenditure is measured and the causes of fatigue, soreness, and
cramps. Part II focuses on how the cardiovascular and respiratory
systems provide oxygen and fuel to the active muscles, how they rid
the body of carbon dioxide and metabolic wastes, and how these
systems respond in an integrated fashion during exercise. In chapter
6, The Cardiovascular System and Its Control, we look at the
structure and function of the cardiovascular system: the heart, blood
vessels, and blood. In chapter 7, The Respiratory System and Its
Regulation, we examine the mechanics and regulation of breathing,
the process of gas exchange in the lungs and at the muscles, and
how oxygen and carbon dioxide are transported to muscles and
other tissues in the blood. We also see how this system regulates
the body’s pH within a very narrow range. Finally, in chapter 8,
Cardiorespiratory Responses to Acute Exercise, we concentrate on
the cardiovascular and respiratory changes that occur during an
acute bout of exercise.
348
349
350
6
The Cardiovascular System and Its
Control
In this chapter and in the web study guide
The Heart
Blood Flow Through the Heart
The Myocardium
The Cardiac Conduction System
The Cardiac Cycle
Determinants of Cardiac Output
ANIMATION FOR FIGURE 6.1 illustrates the course of blood flow through the human heart.
ACTIVITY 6.1 Anatomy of the Heart reviews the names and locations of the structures of the heart.
ACTIVITY 6.2 Functioning of the Heart describes blood flow through the heart and differentiates the
heart’s functions.
AUDIO FOR FIGURE 6.2 describes the mechanism of contraction in a cardiac muscle fiber.
ACTIVITY 6.3 Cardiac Conduction explores the function of each of the components of the heart’s
conduction system.
AUDIO FOR FIGURE 6.6 describes the contributions of the sympathetic and parasympathetic nervous
systems to the rise in heart rate during exercise.
AUDIO FOR FIGURE 6.8 describes the Wiggers diagram.
VIDEO 6.1 presents Ben Levine on torsional contraction of the heart muscle and its role in ventricular
filling.
Vascular System
Blood Pressure
General Hemodynamics
Distribution of Blood
ACTIVITY 6.4 Control of the Vascular System explains the role that parts of the vascular system play
to guarantee an adequate blood supply where it is most needed.
AUDIO FOR FIGURE 6.11 describes the distribution of cardiac output at rest and during maximal
exercise.
AUDIO FOR FIGURE 6.12 describes intrinsic control of blood flow.
351
ANIMATION FOR FIGURE 6.15 shows the action of the muscle pump.
Blood
Blood Volume and Composition
Red Blood Cells
Blood Viscosity
In Closing
352
R
od Williams was a 17-year-old high school junior, an offensive lineman on
the football team. On September 22, 2015, Williams collapsed on the football field
with no heartbeat or respirations. Despite successful CPR and hospitalization, he
died 2 weeks later. Like many tragic, sudden cardiac arrest deaths in young
athletes, an autopsy revealed that Williams had a preexisting heart condition that
went undetected. In fact, sudden cardiac arrest is the leading cause of death in
high school athletes, resulting from underlying heart anomalies that were exposed
only during intense physical activity. The most common of these is hypertrophic
cardiomyopathy, a genetic disease of the heart muscle, but many other causes
exist, such as long QT syndrome, an electrical abnormality. Most young people
living with these problems have no symptoms. Sadly, the initial manifestation is
sudden cardiac arrest. While routine intensive screening seems like the logical
answer, the type of advanced screening that is necessary has significant financial
constraints, since well over 1 million high school football players are competing in
the United States at any one time. Further, because of the low incidence of these
abnormalities in the young, healthy population, the incidences of false positives
(the test shows a problem where there is none) and false negatives (the test is
normal but the problem actually exists) limit the tests’ predictive value. Hopefully,
more accurate and cost-effective screening tools are on the horizon.
The cardiovascular system serves a number of important functions in
the body and supports every other physiological system. Major
cardiovascular functions can be grouped into six categories:
Delivery of oxygen and energy substrates
Removal of carbon dioxide and other metabolic waste
products
Transport of hormones and other molecules
Support of thermoregulation and control of body fluid balance
Maintenance of acid–base balance to help control the body’s
pH
Regulation of immune function
Although this is just an abbreviated list of roles, the cardiovascular
functions listed here are important for understanding the
physiological basis of exercise and sport. Obviously these roles
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change and become even more critical with the challenges imposed
by exercise.
All physiological functions and virtually every cell in the body
depend in some way on the cardiovascular system. Any system of
circulation requires three components:
A pump (the heart)
A system of channels or tubes (the blood vessels)
A fluid medium (the blood)
In order to keep blood circulating, the heart must generate
sufficient pressure to drive blood through the continuous network of
blood vessels in a closed-loop system. Thus, the primary goal of the
cardiovascular system is to ensure that there is adequate blood flow
throughout the circulation to meet the metabolic demands of the
tissues. We look first at the heart.
The Heart
About the size of a fist and located in the center of the thoracic
cavity, the heart is the primary pump that circulates blood through
the entire cardiovascular system. As shown in figure 6.1, the heart
has two atria that act as receiving chambers and two ventricles that
serve as the pumping chambers. It is enclosed in a tough
membranous sac called the pericardium. The thin cavity between
the pericardium and the heart is filled with pericardial fluid, which
reduces friction between the sac and the beating heart.
Blood Flow Through the Heart
The heart is sometimes considered to be two separate pumps, with
the right side of the heart pumping deoxygenated blood to the lungs
through the pulmonary circulation and the left side of the heart
pumping oxygenated blood to all other tissues in the body through
the systemic circulation. Blood that has circulated through the body,
delivering oxygen and nutrients and picking up waste products,
returns to the heart through the great veins—the superior vena cava
and inferior vena cava—to the right atrium. This chamber receives all
the deoxygenated blood from the systemic circulation.
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From the right atrium, blood passes through the tricuspid valve
into the right ventricle. This chamber pumps the blood through the
pulmonary valve into the pulmonary artery, which carries the blood to
the lungs. Thus, the right side of the heart is known as the
pulmonary side, sending the blood that has circulated throughout the
body into the lungs for reoxygenation.
After blood is oxygenated in the lungs, it is transported back to the
heart through the pulmonary veins. All freshly oxygenated blood is
received from the pulmonary veins by the left atrium. From the left
atrium, the blood passes through the mitral valve into the left
ventricle. Blood leaves the left ventricle by passing through the aortic
valve into the aorta and is distributed to the systemic circulation. The
left side of the heart is known as the systemic side. It receives the
oxygenated blood from the lungs and then sends it out to supply all
other body tissues.
FIGURE 6.1 An anterior (as if the person is facing you) cross-sectional view of the human heart.
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The four heart valves prevent backflow of blood, ensuring oneway flow through the heart. These valves maximize the amount of
blood pumped out of the heart during contraction. A heart murmur
is a condition in which abnormal sounds are detected with the aid of
a stethoscope. This abnormal sound can indicate the turbulent flow
of blood through a narrowed valve (stenosis) or retrograde flow back
toward the atria through a leaky valve (prolapse). When valves leak
as a result of disease, this condition can require surgical
replacement of the valve. With mitral valve prolapse, the mitral valve
allows some blood to flow back into the left atrium during ventricular
contraction. This disorder, relatively common in adults (6%-17% of
the population), usually has little clinical significance unless there is
significant backflow.
Mild heart murmurs are fairly common in growing children and
adolescents. Likewise, most murmurs heard in athletes are benign,
affecting neither the heart’s pumping nor the athlete’s performance.
Only when there is a functional consequence, such as lightheadedness or dizziness, are murmurs a cause for immediate
concern.
The Myocardium
Cardiac or myocardial muscle is collectively called the myocardium.
Myocardial thickness at various locations in the heart varies
according to the amount of stress regularly placed on the
myocardium. The left ventricle is the most powerful pump because it
must generate sufficient pressure to pump blood through the entire
body. When a person is sitting or standing, the left ventricle must
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contract with enough force to overcome the effect of gravity, which
tends to pool blood in the lower extremities.
Because the left ventricle must generate considerable force to
pump blood to the systemic circulation, it has the thickest muscular
wall compared with the other heart chambers. This hypertrophy is
the result of the pressure placed on the left ventricle at rest or under
normal conditions of moderate activity. With more vigorous exercise
—particularly intense aerobic activity, during which the working
muscles’ need for blood increases considerably—the demand on the
left ventricle to deliver blood to exercising muscles is much higher. In
response to both intense aerobic and resistance training, the left
ventricle will hypertrophy. In contrast to this positive adaptation that
occurs as a result of exercise training, cardiac muscle also
hypertrophies as a result of several diseases, such as high blood
pressure or valvular heart disease. In response to either training or
disease, over time the left ventricle adapts by increasing its size and
pumping capacity, similar to the way skeletal muscle adapts to
physical training. However, the mechanisms for adaptation and
cardiac performance with disease are different from those observed
with aerobic training.
Although striated in appearance, the myocardium differs from
skeletal muscle in several important ways. First, because the
myocardium has to contract as if it were a single unit, individual
cardiac muscle fibers are anatomically interconnected end to end by
dark-staining regions called intercalated disks. These disks have
desmosomes, which are structures that anchor the individual cells
together so that they do not pull apart during contraction, and gap
junctions, which allow rapid transmission of the action potentials that
signal the heart to contract as one unit. Secondly, the myocardial
fibers are rather homogeneous in contrast to the mosaic of fiber
types in skeletal muscle. The myocardium contains only one fiber
type, similar to type I fibers in skeletal muscle in that it is highly
oxidative, has a high capillary density, and has a large number of
mitochondria.
In addition to these differences, the mechanism of muscle
contraction also differs between skeletal and cardiac muscle.
Cardiac muscle contraction occurs by calcium-induced calcium
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release (figure 6.2). The action potential spreads rapidly along the
myocardial sarcolemma from cell to cell via gap junctions and also to
the inside of the cell through the T-tubules. Upon stimulation, calcium
enters the cell by the dihydropyridine receptor in the T-tubules.
Unlike what happens in skeletal muscle, the amount of calcium that
enters the cell is not sufficient to directly cause the cardiac muscle to
contract, but it serves as a trigger to another type of receptor, called
the ryanodine receptor, to release calcium from the sarcoplasmic
reticulum. Figure 6.3 summarizes some of the similarities and
differences between cardiac and skeletal muscle.
FIGURE 6.2 The mechanism of contraction in a cardiac muscle fiber, termed calcium-induced calcium
release.
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The myocardium, just like skeletal muscle, must have a blood
supply to deliver oxygen and nutrients and remove waste products.
Although blood courses through each chamber of the heart, little
nourishment comes from the blood within the chambers. The primary
blood supply to the heart is provided by the coronary arteries, which
arise from the base of the aorta and encircle the outside of the
myocardium (figure 6.4). The right coronary artery supplies the right
side of the heart, dividing into two primary branches, the marginal
artery and the posterior interventricular artery. The left coronary
artery, also referred to as the left main coronary artery, also divides
into two major branches, the circumflex artery and the anterior
descending artery. The posterior interventricular artery and the
anterior descending artery merge, or anastomose, in the lower
posterior area of the heart, as does the circumflex. Blood flow
increases through the coronary arteries when the heart is between
contractions (during diastole).
The mechanism of blood flow to and through the coronary arteries
is quite different from that of blood flow to the rest of the body. During
contraction, when blood is forced out of the left ventricle under high
pressure, the aortic valve is forced open. When this valve is open, its
flaps block the entrances to the coronary arteries. As the pressure in
the aorta decreases, the aortic valve closes, and blood can then
enter the coronary arteries. This design ensures that the coronary
arteries are spared the very high blood pressure created by
contraction of the left ventricle, thus protecting these critical vessels
from damage.
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FIGURE 6.3 Functional and structural characteristics of skeletal and cardiac muscle.
The coronary arteries are, however, very susceptible to
atherosclerosis, or narrowing by the accumulation of plaque and
inflammation, leading to coronary artery disease. This disease is
discussed in greater detail in chapter 21. Anomalies—vessel
shortenings, blockages, or flow misdirections—sometimes occur in
the coronary arteries, and such congenital abnormalities are a
common cause of sudden death in athletes.
In addition to its unique anatomical structure, the ability of the
myocardium to contract as a single unit also depends on initiation
and propagation of an electrical signal through the heart, the cardiac
conduction system.
The Cardiac Conduction System
Myocardial cells are unique in that they have the ability to
spontaneously depolarize and directionally conduct that electrical
signal throughout the heart. The rate of depolarization is set by
depolarization of a unique type of myocardial cells located in the
upper right atrium and also determined by extrinsic influences,
including the autonomic nervous system and circulating hormones.
The following sections describe the intrinsic and extrinsic
mechanisms that combine to determine heart rate and rhythm at rest
and during exercise.
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FIGURE 6.4 The coronary circulation, illustrating the right and left coronary arteries and their major
branches.
Intrinsic Control of Electrical Activity
Cardiac muscle has the unique ability to generate its own electrical
signal, called spontaneous rhythmicity, which allows it to contract
without any external stimulation. The contraction is rhythmical, in
part because of the anatomical coupling of the myocardial cells
through gap junctions. Without neural or hormonal stimulation, the
intrinsic heart rate averages ~100 beats (contractions) per minute.
This resting heart rate of about 100 beats/min can be observed in
patients who have undergone cardiac transplant surgery, because
their transplanted hearts lack autonomic innervation.
Even though all myocardial fibers have inherent rhythmicity, the
heart has a series of specialized myocardial cells that function to
coordinate the heart’s excitation and contraction and maximize the
efficient pumping of blood. These are specialized cardiac muscle
fibers, and not nerve tissue, even though they function to generate
and transmit a signal. Figure 6.5 illustrates the four main
components of the cardiac conduction system:
Sinoatrial (SA) node
Atrioventricular (AV) node
AV bundle (bundle of His)
Purkinje fibers
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The impulse for a normal heart contraction is initiated in the
sinoatrial (SA) node, a group of specialized fibers located in the
upper posterior wall of the right atrium. These specialized cells
spontaneously depolarize at a faster rate than other myocardial
muscle cells because they are especially leaky to sodium ions.
Because this tissue has the fastest intrinsic firing rate, typically at a
frequency of about 100 beats/min, the SA node is known as the
heart’s pacemaker, and the rhythm it establishes is called the sinus
rhythm. The electrical impulse generated by the SA node spreads
through both atria and reaches the atrioventricular (AV) node,
located in the right atrial wall near the center of the heart. As the
electrical impulse spreads through the atria, the atrial myocardium is
signaled to contract.
The AV node conducts the electrical impulse from the atria into
the ventricles. The impulse is delayed by about 0.13 s as it passes
through the AV node, and then it enters the AV bundle. This delay is
important because it allows blood from the atria to completely empty
into the ventricles to maximize ventricular filling before the ventricles
contract. While most blood moves passively from the atria to the
ventricles, active contraction of the atria (sometimes called the “atrial
kick”) completes the process. The AV bundle travels along the
ventricular septum and then sends right and left bundle branches
into the respective ventricles. These branches send the impulse
toward the apex of the heart and then outward. Each bundle branch
subdivides into many smaller ones that spread throughout the entire
ventricular wall. These terminal branches of the AV bundle are the
Purkinje fibers. They transmit the impulse through the ventricles
approximately six times faster than through the rest of the cardiac
conduction system. This rapid conduction allows all parts of the
ventricle to contract at virtually the same time.
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FIGURE 6.5 The specialized conduction system of the heart.
Occasionally, chronic problems develop within the cardiac
conduction system, hampering its ability to maintain appropriate
sinus rhythm throughout the heart. In such cases, an artificial
pacemaker can be surgically installed. This small, battery-operated
electrical stimulator, usually implanted under the skin, has tiny
electrodes attached to the right ventricle. For example, in a condition
called AV block, the SA node creates an impulse, but the impulse is
blocked at the AV node and cannot reach the ventricles, resulting in
the heart rate’s being controlled by the intrinsic firing rate of the
pacemaker cells in the ventricles (closer to 40 beats/min). The
artificial pacemaker takes over the role of the disabled AV node,
supplying the needed impulse and thus controlling ventricular
contraction.
Extrinsic Control of Heart Rate and Rhythm
Although the heart initiates its own electrical impulses (intrinsic
control), both the heart rate and force of contraction can be altered.
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Under normal conditions, this is accomplished primarily through
three extrinsic systems:
The parasympathetic nervous system
The sympathetic nervous system
The endocrine system (hormones)
Although an overview of these systems’ effects is offered here, they
are discussed in more detail in chapters 3 and 4.
The parasympathetic system, a branch of the autonomic nervous
system, originates centrally in a region of the brain stem called the
medulla oblongata and reaches the heart through the vagus nerve
(cranial nerve X). The vagus nerve carries impulses to the SA and
AV nodes, and when stimulated it releases acetylcholine, which
causes hyperpolarization of the conduction cells. The result is a
slower spontaneous depolarization and a decrease in heart rate. At
rest, parasympathetic system activity predominates and the heart is
said to have “vagal tone.” Recall that, in the absence of vagal tone,
intrinsic heart rate would be approximately 100 beats/min, but the
normal resting adult heart rate is typically 60 to 80 beats/min. The
vagus nerve has a depressant effect on the heart: It slows impulse
generation and conduction and thus decreases the heart rate.
Maximal vagal stimulation can decrease the heart rate to as low as
20 beats/min. The vagus nerve also decreases the force of cardiac
muscle contraction.
The sympathetic nervous system, the other branch of the
autonomic system, has opposite effects. Sympathetic stimulation
increases the rate of depolarization of the SA node as well as
conduction speed, and thus heart rate. Maximal sympathetic
stimulation can increase the heart rate to 250 beats/min.
Sympathetic input also increases the force of contraction of the
ventricles. Sympathetic control predominates during times of
physical or emotional stress when the heart rate is greater than 100
beats/min. The parasympathetic system dominates when heart rate
is less than 100. Thus, when exercise begins, or if exercise is at a
low intensity, heart rate first increases due to withdrawal of vagal
tone, then increases further due to sympathetic activation, as shown
in figure 6.6.
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The third extrinsic influence, the endocrine system, exerts its
effect through two hormones released by the adrenal medulla:
norepinephrine and epinephrine (see chapter 4). These hormones
are also known as catecholamines. Like the norepinephrine released
as a neurotransmitter by the sympathetic nervous system, circulating
norepinephrine and epinephrine stimulate the heart, increasing its
rate and contractility. In fact, release of these hormones from the
adrenal medulla is triggered by sympathetic stimulation during times
of stress, and their actions prolong the sympathetic response.
Normal resting heart rate (RHR) is defined as between 60 and
100 beats/min. With extensive endurance training (over months to
years), RHR can decrease to 35 beats/min or less. A RHR as low as
28 beats/min has been observed in a world-class long-distance
runner. While it has been widely accepted that these lower traininginduced RHRs result primarily from increased parasympathetic
stimulation (vagal tone), the actual mechanisms responsible for this
training-induced sinus bradycardia remain an area of much debate
(see Research Perspective 6.1).
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FIGURE 6.6 Relative contribution of sympathetic and parasympathetic nervous systems to the rise in
heart rate from rest to exercise of increasing intensity.
Adapted from Rowell (1993).
FIGURE 6.7 A graphic illustration of the various phases of the resting electrocardiogram.
Electrocardiogram
The electrical activity of the heart can be recorded to monitor cardiac
changes or diagnose potential cardiac problems. Because body
fluids contain electrolytes, they are good electrical conductors.
Electrical impulses generated in the heart are conducted through
body fluids to the skin, where they can be amplified, detected, and
printed out on an electrocardiograph. This printout is called an
electrocardiogram (ECG). A standard ECG is recorded from 10
electrodes placed in specific anatomical locations. These 10
electrodes correspond to 12 leads that represent different views of
the heart. Three basic components of the ECG represent important
aspects of cardiac function (figure 6.7):
The P wave
The QRS complex
The T wave
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The P wave represents atrial depolarization and occurs when the
electrical impulse travels from the SA node through the atria to the
AV node. The QRS complex represents ventricular depolarization
and occurs as the impulse spreads from the AV bundle to the
Purkinje fibers and through the ventricles. The T wave represents
ventricular repolarization. Atrial repolarization cannot be seen,
because it occurs during ventricular depolarization (QRS complex).
It is important to remember that an ECG measures only the
electrical activity of the heart and does not provide any information
about its function as a pump. Electrocardiograms are often obtained
at rest, then again during exercise as clinical diagnostic tests of
cardiac function. As exercise intensity increases, the heart must beat
faster and work harder to deliver more blood to active muscles.
Indications of coronary artery disease not evident at rest may show
up on the ECG as the strain on the heart increases.
In Review
The atria serve primarily as filling chambers, receiving blood from the veins; the
ventricles are the primary pumps that eject blood from the heart.
Because the left ventricle must produce more force than other chambers to pump
blood throughout the systemic circulation, its myocardial wall is thicker.
Cardiac tissue is capable of spontaneous rhythmicity and has its own specialized
conduction system made up of myocardial fibers that serve specialized functions.
Because it has the fastest inherent rate of depolarization, the SA node is
normally the heart’s pacemaker.
Heart rate and force of contraction can be altered by the autonomic nervous
system (sympathetic and parasympathetic) and the endocrine system through
circulating catecholamines (epinephrine and norepinephrine).
Electrocardiograms are often obtained during exercise as clinical diagnostic tests
of cardiac function. Indications of coronary artery disease not evident at rest may
show up on the ECG as the strain on the heart increases.
The ECG provides no information about the pumping capacity of the heart, only
its electrical activity.
Cardiac Arrhythmias
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Occasionally, disturbances in the normal sequence of cardiac events
can lead to an irregular heart rhythm, called an arrhythmia. These
disturbances vary in degree of seriousness. Bradycardia and
tachycardia are two types of arrhythmias. Bradycardia is defined as
a RHR lower than 60 beats/min, whereas tachycardia is defined as
a resting rate greater than 100 beats/min. With these arrhythmias,
the sinus rhythm is normal, but the rate is altered. In extreme cases,
bradycardia or tachycardia can affect maintenance of blood
pressure. Symptoms of both arrhythmias include fatigue, dizziness,
light-headedness, and fainting. Tachycardia can sometimes be
sensed as palpitations or a racing pulse. Interestingly, highly trained
endurance athletes also develop a resting bradycardia, an
advantageous adaptation. This adaptation should not be confused
with pathological causes of bradycardia. Nor should the elevated
heart rate during exercise be confused with a tachycardia indicative
of underlying disease or dysfunction.
Other arrhythmias may also occur. For example, premature
ventricular contractions (PVCs), which result in the feeling of
skipped or extra beats, are relatively common and result from
impulses originating outside the SA node. Atrial flutter, in which the
atria depolarize at rates of 200 to 400 beats/min, and atrial
fibrillation, in which the atria depolarize in a rapid and uncoordinated
manner, are more serious arrhythmias that may cause ventricular
filling problems. Ventricular tachycardia, defined as three or more
consecutive PVCs, is a very serious arrhythmia that compromises
the pumping capacity of the heart and can lead to ventricular
fibrillation, in which depolarization of the ventricular tissue is
random and uncoordinated. When this happens, the heart is
extremely inefficient, and little or no blood is pumped out of the
heart. Under such conditions, the use of a defibrillator to shock the
heart back into a normal sinus rhythm must occur within minutes if
the victim is to survive.
The Cardiac Cycle
The cardiac cycle includes all the mechanical and electrical events
that occur during one heartbeat. In mechanical terms, all heart
chambers undergo a relaxation phase (diastole) and a contraction
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phase (systole). During diastole, the chambers fill with blood. During
systole, the ventricles contract and expel blood into the aorta and
pulmonary arteries. The diastolic phase is approximately twice as
long as the systolic phase. Consider an individual with a heart rate of
74 beats/min. At this heart rate, the entire cardiac cycle takes 0.81 s
to complete (60 s divided by 74 beats). Of the total cardiac cycle at
this rate, diastole accounts for 0.50 s, or 62% of the cycle, and
systole accounts for 0.31 s, or 38%. As the heart rate increases,
these time intervals shorten proportionately.
RESEARCH PERSPECTIVE 6.1
The Debate Surrounding Exercise Training–Induced
Reductions in Heart Rate
It is well established that endurance exercise training lowers resting heart
rate. Sinus bradycardia (a slow but otherwise normal heart rate) is evident in
endurance athletes, whose resting heart rates can be half of that of their
sedentary age-matched peers. However, despite substantial research, the
mechanisms responsible for this training-induced reduction in resting heart
rate remain an area of much debate.1,2
Two primary hypotheses have been proposed to explain exercise training
–induced reductions in heart rate. The first, termed the autonomic neural
hypothesis, posits that reductions in heart rate result from a shift in autonomic
neural balance (sympathetic versus parasympathetic influences) toward
increased parasympathetic activity. The second, referred to as the intrinsic
rate hypothesis, suggests that changes in inherent cardiac pacemaker rate
(i.e., rate of spontaneous depolarization of the sinoatrial [SA] node cells)
govern reductions in heart rate following training.
Evidence put forth in support of the autonomic neural hypothesis is largely
derived from the indirect evaluation of cardiac autonomic regulation from
changes in heart rate variability or systemic pharmacological interventions
that were not selective to cardiac function. For this hypothesis to be correct,
the selective surgical elimination of cardiac autonomic innervation should
prevent reductions in resting heart rate following exercise training. This has
been demonstrated in an experimental dog model as well as in human
cardiac transplant patients. That is, surgical elimination of all cardiac
innervation completely prevented the exercise training–induced bradycardia.
These data provide direct support for the autonomic neural hypothesis
because they demonstrate that intact autonomic innervation of the heart
(specifically, parasympathetic) is necessary for exercise training to result in
reductions in resting heart rate.
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However, equally convincing data have been set forth in support of the
intrinsic rate hypothesis. With this alternate hypothesis, training bradycardia
results not from increased vagal tone but instead from an electrical
remodeling of the SA node itself. In support of this hypothesis, exercisetrained rodents display downregulation of cardiac ion channels, directly
changing the function of the pacemaker of the heart, the SA node.
Furthermore, prevention of ion channel downregulation abolished the
difference in heart rate between trained and untrained animals. When
considered collectively, these data provide support for the concept that
alterations in SA node function mediate training-induced reductions in heart
rate.
Regardless of whether the autonomic neural hypothesis or the intrinsic
rate hypothesis, or a synthesis of the two, is ultimately proven correct, this
ongoing debate highlights the critical importance of the scientific method in
reaching these conclusions. That is, experiments must be conducted to test a
specific hypothesis, and these experiments must be well controlled and
adequately powered in order for the results to advance scientific discussion
and discovery.
Refer to the normal ECG in figure 6.7. One cardiac cycle spans
the time between one systole and the next. Ventricular contraction
(systole) begins during the QRS complex and ends in the T wave.
Ventricular relaxation (diastole) occurs during the T wave and
continues until the next contraction. Although the heart is continually
working, it spends slightly more time in diastole (~2/3 of the cardiac
cycle) than in systole (~1/3 of the cardiac cycle).
The pressure inside the heart chambers rises and falls during
each cardiac cycle. When the atria are relaxed, blood from the
venous circulation fills the atria. About 70% of the blood filling the
atria during this time passively flows directly through the mitral and
tricuspid valves into the ventricles. When the atria contract, the atria
push the remaining 30% of their volume into the ventricles.
During ventricular diastole, the pressure inside the ventricles is
low, allowing the ventricles to passively fill with blood. As atrial
contraction provides the final filling volume of blood, the pressure
inside the ventricles increases slightly. As the ventricles contract,
pressure inside the ventricles rises sharply. This increase in
ventricular pressure forces the atrioventricular valves (i.e., tricuspid
and mitral valves) closed, preventing any backflow of blood from the
ventricles to the atria. The closing of the atrioventricular valves
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results in the first heart sound. Then, when ventricular pressure
exceeds the pressure in the pulmonary artery and the aorta, the
pulmonary and aortic valves open, allowing blood to flow into the
pulmonary and systemic circulations, respectively. Following
ventricular contraction, pressure inside the ventricles falls and the
pulmonary and aortic valves close. The closing of these valves
corresponds to the second heart sound. The two sounds together,
the result of valves closing, results in the typical “lub, dub” heard
through a stethoscope during each heartbeat.
The interactions of the various events that take place during one
cardiac cycle are illustrated in figure 6.8, called a Wiggers diagram
after the physiologist who created it. The diagram integrates
information from the electrical conduction signals (ECG), heart
sounds from the heart valves, pressure changes within the heart
chambers, and left ventricular volume.
FIGURE 6.8 The Wiggers diagram, illustrating the events of the cardiac cycle for left ventricular
function. Integrated into this diagram are the changes in left atrial and ventricular pressure, aortic
pressure, ventricular volume, electrical activity (electrocardiogram), and heart sounds.
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Determinants of Cardiac Output
The heart’s primary function is as a pump. The volume of blood
pumped by the heart each minute governs blood flow to living
tissues and, in the case of working muscle, is a key determinant of
exercise performance.
Stroke Volume
During systole, most, but not all, of the blood in the ventricles is
ejected. This volume of blood pumped during one beat (contraction)
is the stroke volume (SV). This is depicted in figure 6.9a. To
understand SV, consider the amount of blood in the ventricle before
and after contraction. At the end of diastole, just before contraction,
the ventricle has finished filling. The volume of blood it now contains
is called the end-diastolic volume (EDV). At rest in a normal
healthy adult, this value is approximately 100 ml. At the end of
systole, just after the contraction, the ventricle has completed its
ejection phase, but not all the blood is pumped out of the heart. The
volume of blood remaining in the ventricle is called the end-systolic
volume (ESV) and is approximately 40 ml under resting conditions.
Stroke volume is the volume of blood that was ejected and is merely
the difference between the volume of the filled ventricle and the
volume remaining in the ventricle after contraction. So, SV is simply
the difference between EDV and ESV; that is, SV = EDV − ESV
(example: SV = 100 ml − 40 ml = 60 ml).
Ejection Fraction
The fraction of the blood pumped out of the left ventricle in relation to
the amount of blood that was in the ventricle before contraction is
called the ejection fraction (EF). Ejection fraction is determined by
dividing the SV by EDV (60 ml / 100 ml = 60%), as in figure 6.9b.
The EF, generally expressed as a percentage, averages about 60%
at rest in healthy, active young adults. Thus, 60% of the blood in the
ventricle at the end of diastole is ejected with the next contraction,
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and 40% remains in the ventricle. Ejection fraction is often used
clinically as an index of the pumping ability of the heart.
FIGURE 6.9 Calculations of stroke volume, ejection fraction, and cardiac output based on volumes of
blood flowing into and out of the heart.
Cardiac Output
Cardiac output ( ), as shown in figure 6.9c, is the total volume of
blood pumped by the ventricle per minute, the product of heart rate
(HR) and SV. The SV at rest in the standing posture averages
between 60 and 80 ml of blood in most adults. Thus, at a RHR of 70
beats/min, the resting cardiac output will vary between 4.2 and 5.6
L/min. The average adult body contains about 5 L of blood, so this
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means that the equivalent of our total blood volume is pumped
through our hearts about once every minute.
Pumping Action of the Heart During Exercise
As described earlier in this chapter, the myocardium has to contract
as if it were a single unit in order to efficiently pump blood. For that
reason, myocardial cells are anatomically interconnected end to end
by intercalated disks that anchor the individual cells together so that
they do not pull apart during contraction. This better allows the heart
to contract as one unit, often called a functional syncytium.
VIDEO 6.1 Presents Ben Levine on torsional contraction of the
heart muscle and its role in ventricular filling.
During intense exercise when heart rates are high, the time
available between contractions for diastolic filling is very short. Yet
complete filling of the left ventricle must occur in order to
appropriately increase cardiac output. The heart actually uses the
increased contractility that occurs during exercise to enhance left
ventricle filling, a process called torsional contraction. As the heart
beats, contraction and relaxation of the atria and the ventricles
create a twisting and untwisting action, similar to wringing out a
towel. During systole (contraction), the heart twists gradually, storing
energy and compressing the springlike titin molecules in the
sarcomere (see chapter 1 for a description of titin’s similar role in
skeletal muscle). When the aortic valve closes, the ventricle abruptly
untwists. This recoil creates a 1 to 2 mmHg pressure difference
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between the base (top) and apex (bottom) of the heart, which pulls
blood from the atrium, across the mitral valve, and into the ventricle.
RESEARCH PERSPECTIVE 6.2
Can Too Much Exercise Be Bad for Your Heart?
It is well known that habitual physical activity reduces cardiovascular disease
risk and that exercise dose is also important; higher physical activity levels
further reduce mortality risk, and the most active individuals demonstrate the
highest overall life expectancy. However, few studies have included
individuals engaging in lifelong high-intensity endurance exercise. This is an
important gap in our knowledge, since recent evidence suggests that such
intense exercise may paradoxically increase cardiovascular risk.
Intense exercise performed regularly elicits structural, functional, and
electrical cardiac adaptations, collectively known as the athlete’s heart. As
elegantly reviewed by Eijsvogels and colleagues,8 these adaptations may
also impart deleterious effects. In response to exercise training, all four
chambers of the heart enlarge. Although this adaptation facilitates exercise
performance, it may also have adverse cardiac effects. For example, atrial
fibrillation becomes more common, potentially resulting from increased vagal
tone and left atrial size. Further, right ventricular wall stress is increased,
possibly due to exercise-induced increases in pulmonary artery systolic
pressure. Together, these changes in heart structure may hasten cardiac
disease in susceptible individuals.
In addition to structural adaptations, exercise also acutely increases
circulating biomarkers for cardiovascular disease, including creatine kinase,
cardiac troponin, and B-type natriuretic peptide. Although the source of these
circulating molecules remains unclear, the increases likely result from both
skeletal muscle damage and stress-activated cardiac muscle. These
increases may be cause for concern because prolonged exercise reduces
ventricular function and acutely injures cardiac muscle, resulting in cardiac
fatigue. Myocardial fibrosis (a buildup of scar tissue in the cardiac muscle or
valves) has also been documented in some lifelong endurance athletes. The
interrelation between increases in cardiac biomarkers, reductions in
ventricular function, and cardiac fibrosis may impart increased risk, though
the precise mechanisms remain incompletely understood.
While the possibility that lifelong intense endurance exercise may
increase cardiac risk cannot be ignored, for the majority of the population, the
evidence supporting the beneficial cardiovascular outcomes attributed to
exercise and physical activity is overwhelming. It is these health benefits that
led to the development of strategies to increase physical activity, with very
specific guidelines put forth by both the American College of Sports Medicine
and the American Heart Association. Unfortunately, the majority of Americans
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fail to meet these exercise criteria, putting themselves at an ever-increased
risk of cardiovascular disease.
The torsion during systole stores energy that is then released
during isovolumetric relaxation (the period during the cardiac cycle
after contraction when all of the valves are closed and the
myocardium is relaxing) to generate the diastolic suction that allows
enhanced atrial filling during exercise. This twisting action is
enhanced almost threefold during exercise and assists in efficient
ventricular filling. This left ventricle twisting and rapid untwisting,
inducing diastolic suction in the ventricle, is called dynamic
relaxation.10 Cardiac twisting mechanics are improved with exercise
training and reduced by detraining.7
In Review
The electrical and mechanical events that occur in the heart during one heartbeat
make up one cardiac cycle. A Wiggers diagram depicts the intricate timing of
these events.
Cardiac output, the volume of blood pumped by each ventricle per minute, is the
product of HR and SV.
Not all of the blood in the ventricles is ejected during systole. The ejected volume
is the SV, while the percentage of blood pumped with each beat is the EF.
To calculate SV, EF, and cardiac output:
SV (ml/beat) = EDV – ESV
EF (%) = (SV/EDV) × 100
(L/min) = HR × SV
As the heart beats, contraction and relaxation of the atria and the ventricles
create a twisting and untwisting action that allows the ventricles to fill even at
high heart rates.
Understanding the electrical and mechanical activity of the heart
provides a basis for understanding the cardiovascular system, but
the heart is only one part of this system. In addition to this pump, the
cardiovascular system contains an intricate network of tubes that
serve as a delivery system carrying the blood to all body tissues.
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Vascular System
The vascular system contains a series of vessels that transport
blood from the heart to the tissues and back: the arteries, arterioles,
capillaries, venules, and veins.
Arteries are large, muscular, elastic conduit vessels for
transporting blood away from the heart to the arterioles. The aorta is
the largest artery, transporting blood from the left ventricle to all
regions of the body as it eventually branches into smaller and
smaller arteries, finally branching into arterioles. The arterioles are
the site of greatest control of the circulation by the sympathetic
nervous system, so arterioles are sometimes called resistance
vessels. Arterioles are heavily innervated by the sympathetic
nervous system and are the main site of control of blood flow to
specific tissues.
From the arterioles, blood enters the capillaries, the narrowest
and simplest vessels in terms of their structure, with walls only one
cell thick. Virtually all exchange between the blood and the tissues
occurs at the capillaries. Blood leaves the capillaries to begin the
return trip to the heart in the venules, and the venules form larger
vessels—the veins. The vena cava is the great vein transporting
blood back to the right atrium from all regions of the body above
(superior vena cava) and below (inferior vena cava) the heart.
Blood Pressure
Blood pressure is the pressure exerted by the blood on the arterial
walls. It is expressed by two numbers: the systolic blood pressure
(SBP) and the diastolic blood pressure (DBP). The higher number
is the SBP; it represents the highest pressure in the artery that
occurs during ventricular systole. Ventricular contraction pushes the
blood through the arteries with tremendous force, and that force
exerts high pressure on the arterial walls. The lower number is the
DBP and represents the lowest pressure in the artery, corresponding
to ventricular diastole when the ventricle is filling.
Mean arterial pressure (MAP) represents the average pressure
exerted by the blood as it travels through the arteries. Since diastole
takes about twice as long as systole in a normal cardiac cycle, MAP
can be estimated from the DBP and SBP as follows:
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MAP = 2/3 DBP + 1/3 SBP
Alternatively,
MAP = DBP + [0.333 × (SBP − DBP)]
(SBP − DBP) is also called pulse pressure.
To illustrate, with a normal resting blood pressure of 120 mmHg
over 80 mmHg, the MAP = 80 + [0.333 × (120 − 80)] = 93 mmHg.
General Hemodynamics
The cardiovascular system is a continuous closed-loop system.
Blood flows through this closed loop because of the pressure
gradient that exists between the arterial and venous sides of the
circulation. To understand regulation of blood flow to the tissues, it is
necessary to understand the intricate relationship between pressure,
blood flow, and resistance.
In order for blood to flow through a vessel, there must be a
pressure difference from one end of the vessel to the other end.
Blood will flow from the region of the vessel with high pressure to the
region of the vessel with low pressure. Alternatively, if there is no
pressure difference across the vessel, there is no driving force and
therefore no blood flow. In the circulatory system, the MAP in the
aorta is approximately 100 mmHg at rest, and the pressure in the
right atrium is very close to 0 mmHg. Therefore, the pressure
difference across the entire circulatory system is 100 mmHg − 0
mmHg = 100 mmHg.
The reason for the pressure differential from the arterial to the
venous circulation is that the blood vessels themselves provide
resistance to blood flow. The resistance that the vessel provides is
largely dictated by the properties of the blood vessel and the blood
itself. These properties include the length and radius of the blood
vessel and the viscosity or thickness of the blood flowing through the
vessel. Resistance to flow can be calculated as
Resistance = η × L / r4
where η is the viscosity (thickness) of the blood, L is the length of the
vessel, and r is the radius of the vessel, which is raised to the fourth
power. Blood flow is proportional to the pressure difference across
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the system and is inversely proportional to resistance. This
relationship can be illustrated by the following equation:
Blood flow = ∆pressure / resistance
Notice that blood flow can increase by either an increase in the
pressure difference (∆pressure), a decrease in resistance, or a
combination of the two. Altering resistance to control blood flow is
much more advantageous because very small changes in blood
vessel radius equate to large changes in resistance. This is due to
the fourth-power mathematical relationship between vascular
resistance and vessel radius.
Changes in vascular resistance are largely due to changes in the
radius or diameter of the vessels, since the viscosity of the blood and
the length of the vessels do not change significantly under normal
conditions. Therefore, regulation of blood flow to organs is
accomplished by small changes in vessel radius through
vasoconstriction and vasodilation. This allows the cardiovascular
system to divert blood flow to the areas where it is needed most.
As mentioned earlier, most resistance to blood flow occurs in the
arterioles. Figure 6.10 shows the blood pressure changes across the
entire vascular system. The arterioles are responsible for ~70% to
80% of the drop in MAP across the entire cardiovascular system.
This is important because small changes in arteriole radius can
greatly affect the regulation of mean arteriole pressure and the local
control of blood flow. At the capillary level, changes due to systole
and diastole are no longer evident, and the flow is smooth (laminar)
rather than turbulent.
In Review
Systolic blood pressure is the highest pressure within the vascular system,
whereas DBP is the lowest pressure.
Mean arterial pressure is the average pressure on the vessel walls during a
cardiac cycle; however, it is not the mathematical mean of SBP and DBP
because diastole takes about twice as long as systole.
In terms of the entire cardiovascular system, cardiac output is the blood flow to
the entire system, the ∆pressure is the difference between aortic pressure when
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blood leaves the heart and venous pressure when blood returns to the heart, and
resistance is the impedance to blood flow from the blood vessels.
Blood flow is mainly controlled by small changes in blood vessel (arteriole) radius
that greatly change resistance.
Distribution of Blood
Distribution of blood to the various body tissues varies considerably
depending on the immediate needs of a specific tissue compared
with those of other areas of the body. As a general rule, the most
metabolically active tissues receive the greatest blood supply. At rest
under normal conditions, the liver and kidneys combine to receive
approximately half of the cardiac output, while resting skeletal
muscles receive only about 15% to 20%.
During exercise, blood is redirected to the areas where it is
needed most. During heavy endurance exercise, contracting
muscles may receive 80% or more of the blood flow, and flow to the
liver and kidneys decreases. This redistribution, along with increases
in cardiac output (discussed in chapter 8), allows up to 25 times
more blood flow to active muscles (see figure 6.11).
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FIGURE 6.10 Pressure changes across the systemic circulation. Notice the large pressure drop that
occurs across the arteriole portion of the system.
Alternatively, after one eats a big meal, the digestive system
receives more of the available cardiac output than when the
digestive system is empty. Along the same lines, during increasing
environmental heat stress, skin blood flow increases to a greater
extent as the body attempts to maintain normal temperature. The
cardiovascular system responds accordingly to redistribute blood,
whether it is to the exercising muscle to match metabolism, for
digestion, or to facilitate thermoregulation. These changes in the
distribution of cardiac output are controlled by the sympathetic
nervous system, primarily by increasing or decreasing the diameter
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of the arterioles providing blood flow to the given tissue or organ.
Arterioles have a strong muscular wall that can significantly alter
vessel diameter, are highly innervated by sympathetic nerves, and
have the capacity to respond to local control mechanisms.
Intrinsic Control of Blood Flow
Intrinsic control of blood distribution refers to the ability of the local
tissues to dilate or constrict the arterioles that serve them and alter
regional blood flow depending on the immediate needs of those
tissues. With exercise and the increased metabolic demand of the
exercising skeletal muscles, the arterioles undergo intrinsic
vasodilation, opening up to allow more blood to enter the highly
active tissue.
FIGURE 6.11 Distribution of cardiac output at rest and maximal exercise.
*Depends on ambient and body temperatures.
Reprinted by permission from P.O. Åstrand et al., Textbook of Work Physiology: Physiological Bases of Exercise,
4th ed. (Champaign, IL: Human Kinetics, 2003), 143.
There are essentially three types of intrinsic control of blood flow.
Metabolic regulation, in response to an increased oxygen demand, is
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the strongest stimulus for the release of local vasodilating chemicals.
As oxygen uptake by metabolically active tissues increases,
available oxygen is diminished. Local arterioles dilate to allow more
blood to perfuse the area, delivering more oxygen. Other chemical
changes that can stimulate increased blood flow are decreases in
other nutrients and increases in by-products (carbon dioxide, K+, H+,
lactic acid) or inflammatory molecules.
Second, many dilator substances can be produced within the
endothelium (inner lining) of arterioles that can initiate vasodilation in
the vascular smooth muscle of those arterioles (endotheliummediated vasodilation). These substances include nitric oxide (NO),
prostaglandins, and endothelium-derived hyperpolarizing factor
(EDHF). These endothelium-derived vasodilators are important
regulators of blood flow at rest and during exercise in humans.
Additionally, acetylcholine and adenosine have been proposed as
potential vasodilators for the increase in muscle blood flow during
exercise.
Third, pressure changes within the vessels themselves can also
cause vasodilation and vasoconstriction. This is referred to as the
myogenic response. The vascular smooth muscle contracts in
response to an increase in pressure across the vessel wall and
relaxes in response to a decrease in pressure across the vessel wall.
Figure 6.12 illustrates the three types of intrinsic control of vascular
tone.
Extrinsic Neural Control
The concept of intrinsic local control explains redistribution of blood
within an organ or tissue; however, the cardiovascular system must
divert blood flow to where it is needed, beginning at a site upstream
of the local environment. Redistribution at the system or organ level
is controlled by neural mechanisms. This is known as extrinsic
neural control of blood flow, because the control comes from
outside the specific area (extrinsic) instead of from inside the tissues
(intrinsic).
Blood flow to all body parts is regulated largely by the sympathetic
nervous system. Sympathetic nerves are abundant in the circular
layers of smooth muscle within the artery and arteriole walls. In most
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vessels, an increase in sympathetic nerve activity causes these
circular smooth muscle cells to contract, constricting blood vessels
and thereby decreasing blood flow.
Under normal resting conditions, sympathetic nerves transmit
impulses continuously to the blood vessels (in particular, the
arterioles), keeping the vessels moderately constricted to maintain
adequate blood pressure. This state of tonic vasoconstriction is
referred to as vasomotor tone. When sympathetic stimulation
increases, further constriction of the blood vessels in a specific area
decreases blood flow into that area and allows more blood to be
distributed elsewhere. But if sympathetic stimulation decreases
below the level needed to maintain tone, constriction of vessels in
the area is lessened, so the vessels passively dilate, increasing
blood flow into that area. Therefore, sympathetic stimulation will
cause vasoconstriction in most vessels. Blood flow can passively be
increased through a lowering of the normal tonic level of sympathetic
outflow.
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FIGURE 6.12 Intrinsic control of blood flow. Arterioles are signaled to dilate or constrict at the local
level (a) by changes in the local concentration of oxygen or metabolic products, (b) by the effects of
local pressure within the arterioles, and (c) by endothelium-derived factors.
Figure courtesy of Dr. Donna H. Korzick, Pennsylvania State University.
Local Control of Muscle Blood Flow
The previous two sections discuss intrinsic and extrinsic control of
blood flow, mechanisms that pertain to controlling flow to all tissues
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of the body. However, muscle blood flow deserves special attention
because (1) contracting muscle is the hallmark response of exercise
physiology and (2) unique mechanisms exist to support increased
muscle blood flow. During aerobic exercise, blood flow to exercising
muscle must increase to match the metabolic demand of that
muscle. Enhanced oxygen delivery to exercising muscle can occur
via a number of different mechanisms, including local alteration of
blood flow, improved oxygen extraction at the tissue level, or both.
Exercise is accompanied by a general increase in sympathetic
nerve activity, including that directed to muscle, which causes
vasoconstriction. How does working muscle overcome systemic
vasoconstriction and actually increase blood flow? The primary
mechanism is termed functional sympatholysis. Vasoactive
molecules released from the active skeletal muscle and endothelium
have been shown to inhibit sympathetic vasoconstriction by reducing
vascular responsiveness to α-adrenergic receptor activation.
Endothelial cells release molecules called endothelial-derived
hyperpolarizing factors (EDHFs) that make it more difficult for
smooth muscle cells to constrict in response to sympathetic
stimulation. For example, we now know that ATP released from the
endothelium and from red blood cells can cause hyperpolarization of
vascular smooth muscle cells that helps override α-adrenergic
vasoconstriction. Functional sympatholysis helps optimize muscle
blood flow distribution to match tissue perfusion with metabolic
demand.
When oxygen availability is limited under conditions of reduced
arterial O2 content (e.g., hypoxia) or decreased perfusion pressure,
the skeletal muscle arterioles dilate to compensate for reduced O2
delivery, allowing for a greater O2 extraction at the tissue level.4 This
phenomenon is termed compensatory vasodilation.
In order to examine the mechanisms by which the local control of
skeletal muscle blood flow is altered in exercising muscle in humans,
investigators have used acute systemic hypoxia, usually by having
subjects breathe air mixtures with a low O2 content, to reduce arterial
O2 content during exercise11 or have temporarily limited blood flow to
the exercising muscle by partially occluding flow to the exercising
limb. During submaximal hypoxic exercise, blood flow to the
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exercising muscle is the same as that seen during normoxic exercise
due to the individual and combined roles of β-adrenergic receptors,
adenosine, and nitric oxide (NO), as shown in figure 6.13.
Interestingly, the contribution of these different dilator mechanisms
can change, depending on the exercise intensity and whether blood
flow to the exercising muscle is limited. For example, during lowintensity exercise under hypoxic conditions, stimulation of βadrenergic receptors contributes to vasodilation; however, as
exercise intensity increases, NO release from the endothelium
contributes to a greater extent in the compensatory vasodilator
response.3 The molecule adenosine can also contribute to
compensatory vasodilation, especially under conditions in which
blood flow is limited. At higher exercise intensities in which the
muscle fibers’ oxygen needs are even greater, NO and several other
vasodilator molecules, including prostaglandins and adenosine
triphosphate (ATP), mediate vasodilation. However, there are
redundancies in these vasodilator mechanisms, such that when one
is blocked or downregulated, another vasodilator can compensate
and cause vasodilation.
RESEARCH PERSPECTIVE 6.3
Vascular Adaptations to Exercise
Postmenopausal Women
Training
in
Despite recent declines in prevalence, cardiovascular disease remains the
leading cause of death in the United States. Interestingly, cardiovascular
mortality risk differs greatly between the sexes. The establishment of the
National Institutes of Health (NIH) Office of Women’s Health Research in
1990 and the passage of the NIH Revitalization Act in 1993 mandated the
inclusion of women in NIH-funded research. Since the adoption of these
requirements, much has been learned about the mechanisms and
manifestation of cardiovascular disease in women. Yet despite these
advancements, the reasons for the sex disparity in cardiovascular morbidity
and mortality remain unclear.
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Estrogen is required to elicit exercise training–induced improvements in vascular
endothelial function in older postmenopausal women. In older men, moderateintensity exercise training significantly improves vascular function, as assessed by
endothelium-dependent dilation. This beneficial vascular adaptation to exercise did
not occur in a group of postmenopausal women of similar age. However, when
postmenopausal women were supplemented with estrogen, the expected
improvements in vascular endothelial function following exercise training were similar
to those observed in age-matched men.
Vascular aging (age-related changes in blood vessels) is considered a
primary risk factor for age-associated cardiovascular disease. Endothelial
dysfunction, defined as impaired endothelium-dependent dilation, is the first
functional manifestation of atherosclerosis and accelerates the progression of
cardiovascular disease. Lifestyle modifications, such as habitual physical
activity, are commonly recommended as a first-line strategy to mitigate ageassociated declines in vascular endothelial function. However, there is now
an increasing awareness of potential sex differences in the beneficial effects
of exercise training on vascular health in older, postmenopausal women.
In a 2006 review of the prevailing literature, researchers provided support
for the notion that sex hormones, specifically estrogen, modulate the exercise
training–induced improvements in vascular function in women.11 That is, the
reduction in estrogen that occurs during menopause consequently prevents
improvements in vascular function with exercise training, as highlighted in the
accompanying figure. As expected, in previously sedentary middle-aged and
older men, a moderate-intensity exercise training program significantly
improved vascular function. In contrast, this exercise training paradigm had
no effect in older postmenopausal women. However, in sedentary
postmenopausal women treated with estrogen, a moderate-intensity training
program did significantly improve vascular endothelial function. These
findings have been corroborated in studies using varied methodology, and
provide direct evidence suggesting that estrogen is required for traininginduced improvements in vascular function in postmenopausal women.
Given the rapidly aging population, effective preventive strategies to
mitigate the untoward consequences of cardiovascular disease are
paramount. Habitual physical activity is an important strategy for the primary
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prevention of cardiovascular disease—in men and women. Yet, it is
exceedingly apparent that the vasculature of older men and women responds
differently to exercise training, and this differential responsiveness can likely
be attributed to sex hormones, or the lack thereof. Further research is
necessary to determine if additional pharmacological or nonpharmacological
strategies should be coupled with exercise training in order to provide a
viable therapeutic intervention that permits improvements in vascular
endothelial function during exercise training in estrogen-deficient
postmenopausal women.
FIGURE 6.13 The proposed mechanisms for functional sympatholysis and hypoxia-induced
vasodilation during exercise. During hypoxic exercise, nitric oxide (NO) is the final common pathway for
the compensatory dilator response. Systemic epinephrine (E) release, acting via β-adrenergic
receptors, contributes to the NO-mediated vasodilation at lower exercise intensities, but this βadrenergic contribution decreases with increasing exercise intensity. Adenosine triphosphate (ATP)
released from the red blood cell (RBC), endothelial-derived prostacyclin (PGI2), or both remain, also
stimulating NO during higher-intensity hypoxic exercise. α1AR, α2AR, and β2AR = α1-, α2-, and β2adrenergic receptors, respectively; NE = norepinephrine; PR = purinergic receptors that are stimulated
by ATP; ADO = adenosine.
Because of the biological importance of NO, these mechanisms
have significant implications in clinical populations such as older
individuals and patients with cardiovascular disease, in whom NO
production and availability may be limited.5,6 For example, as
humans age, there is a reduction in NO synthesis and an increase in
NO breakdown, and compensatory vasodilation is blunted in healthy
older humans.11
Distribution of Venous Blood
While flow to tissues is controlled by changes on the arterial side of
the system, most of the blood volume resides in the venous side of
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the system. At rest, the blood volume is distributed among the
vasculature as shown in figure 6.14. The venous system has a great
capacity to store blood volume because veins have little vascular
smooth muscle and are very elastic and balloon-like. Thus, the
venous system provides a large reservoir of blood available to be
rapidly distributed back to the heart (venous return) and from there to
the arterial circulation. This is accomplished through sympathetic
stimulation of the venules and veins, which causes the vessels to
constrict (venoconstriction).
FIGURE 6.14 Blood volume distribution within the vasculature when the body is at rest.
Integrative Control of Blood Pressure
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Blood pressure is controlled by reflexes. Specialized pressure
sensors located in the aortic arch and the carotid arteries, called
baroreceptors, are sensitive to changes in arterial pressure. When
the pressure in these large arteries changes, afferent signals are
sent to the cardiovascular control centers in the brain where
autonomic reflexes are initiated, and efferent signals are sent to
respond to changes in blood pressure. For example, when blood
pressure is elevated, the baroreceptors are stimulated by an
increase in stretch. They relay this information to the cardiovascular
control center in the brain. In response to the increased pressure is
an increase in vagal tone, which decreases heart rate, and a
decrease in sympathetic activity to both the heart and the arterioles,
which causes the arterioles to dilate. All of these adjustments serve
to decrease blood pressure back to normal. In response to a
decrease in blood pressure, less stretch is sensed by the
baroreceptors, and the response is to increase heart rate (vagal
withdrawal) and constrict arterioles (through increased sympathetic
nervous activity), thus correcting the low-pressure signal.
Other specialized receptors, called chemoreceptors and
mechanoreceptors, send information about the chemical
environment in the muscle and the length and tension of the muscle,
respectively, to the cardiovascular control centers. These receptors
also modify the blood pressure response and are especially
important during exercise.
Return of Blood to the Heart
Because humans spend so much time in an upright position, the
cardiovascular system requires mechanical assistance to overcome
the force of gravity and assist the return of venous blood from the
lower parts of the body to the heart. Three basic mechanisms assist
in this process:
Valves in the veins
The muscle pump
The respiratory pump
The veins contain valves that allow blood to flow in only one
direction, thus preventing backflow and further pooling of blood in the
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lower body. These venous valves also complement the action of the
skeletal muscle pump, the rhythmic mechanical compression of the
veins that occurs during the rhythmic skeletal muscle contraction
accompanying many types of movement and exercise, for example,
during walking and running (figure 6.15). The muscle pump pushes
blood volume in the veins back toward the heart. Finally, changes in
pressure in the abdominal and thoracic cavities during breathing
assist blood return to the heart by creating a pressure gradient
between the veins and the chest cavity.
FIGURE 6.15 The muscle pump. As the skeletal muscles contract, they squeeze the veins in the legs
and assist in the return of blood to the heart. Valves within the veins ensure the unidirectional flow of
blood back to the heart.
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In Review
Blood is distributed throughout the body based primarily on the metabolic needs
of the individual tissues. The most active tissues receive the highest blood flow.
Skeletal muscle normally receives about 15% of the cardiac output at rest. This
can increase to 80% or more during heavy endurance exercise.
Redistribution of blood flow is controlled locally by the release of dilators from
either the tissue (metabolic regulation) or the endothelium of the blood vessel
(endothelium-mediated dilation). A third type of intrinsic control involves the
response of the arteriole to pressure. Decreased arteriolar pressure causes
vasodilation, thus increasing blood flow to the area, while increased pressure
causes local constriction.
Extrinsic neural control of blood flow distribution is accomplished by the
sympathetic nervous system, primarily through vasoconstriction of small arteries
and arterioles.
During aerobic exercise, blood flow to exercising muscle must increase to match
the metabolic demand of that muscle. This is accomplished by (1) functional
sympatholysis (which overcomes sympathetic vasoconstriction) and (2)
compensatory vasodilation (involving molecules such as adenosine and nitric
oxide).
Blood pressure is maintained under normal conditions by reflexes within the
autonomic system.
Blood returns to the heart through the veins, assisted by valves within the veins,
the muscle pump, and changes in respiratory pressure.
Blood
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Blood serves many diverse purposes in regulating normal body
function. The three functions of primary importance to exercise and
sport are
transportation,
temperature regulation, and
acid–base (pH) balance.
We are most familiar with blood’s transporting functions, delivering
oxygen and fuel substrates and carrying away metabolic byproducts. In addition, blood is critical in temperature regulation
during physical activity because it picks up heat from the exercising
muscle and delivers it to the skin, where it can be dissipated to the
environment (see chapter 12). Blood also buffers the acids produced
by anaerobic metabolism and maintains proper pH for metabolic
processes (see chapters 2 and 7).
Blood Volume and Composition
The total volume of blood in the body varies considerably with an
individual’s size, body composition, and state of training. Larger
blood volumes are associated with greater lean body mass and
higher levels of endurance training. The blood volume of people of
average body size and normal physical activity generally ranges
from 5 to 6 L in men and 4 to 5 L in women.
Blood is composed of plasma and formed elements (see figure
6.16). Plasma normally constitutes about 55% to 60% of total blood
volume but can decrease by 10% of its normal amount or more with
intense exercise in hot conditions, or can increase by 10% or more
with endurance training or acclimation to heat. Approximately 90% of
the plasma volume is water; 7% consists of plasma proteins; and the
remaining 3% includes cellular nutrients, electrolytes, enzymes,
hormones, antibodies, and wastes.
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FIGURE 6.16 (a) The composition of whole blood, illustrating the plasma volume (fluid portion) and
the cellular volume (red cells, white cells, and platelets) after the blood sample has been centrifuged to
separate its components. (b) A centrifuge.
The formed elements, which normally constitute the other 40% to
45% of total blood volume, are the red blood cells (erythrocytes),
white blood cells (leukocytes), and platelets (thrombocytes). Red
blood cells constitute more than 99% of the formed-element volume;
white blood cells and platelets together account for less than 1%.
The percentage of the total blood volume composed of cells or
formed elements is referred to as the hematocrit. Hematocrit varies
among individuals, but a normal range is 41% to 50% in adult men
and 36% to 44% in adult women.
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White blood cells protect the body from infection either by directly
destroying the invading agents through phagocytosis (ingestion) or
by forming antibodies to destroy them. Adults have about 7,000
white blood cells per cubic millimeter of blood.
The remaining formed elements are the blood platelets. These are
cell fragments that are required for blood coagulation (clotting),
which prevents excessive blood loss. Exercise physiologists are
most concerned with red blood cells.
Red Blood Cells
Mature red blood cells (erythrocytes) have no nucleus, so they
cannot reproduce as other cells can. They must be replaced with
new cells on a recurring basis, a process called hematopoiesis. The
normal life span of a red blood cell is about 4 months. Thus, these
cells are continuously produced and destroyed at equal rates. This
balance is very important, because adequate oxygen delivery to
tissues depends on having a sufficient number of red blood cells to
transport oxygen. Decreases in their number or function can hinder
oxygen delivery and thus affect exercise performance.
When we donate blood, the removal of one unit, or nearly 500 ml,
represents approximately an 8% to 10% reduction in both the total
blood volume and the number of circulating red blood cells. Donors
are advised to drink plenty of fluids. Because plasma is primarily
water, simple fluid replacement returns plasma volume to normal
within 24 to 48 h. However, it takes at least 6 weeks to reconstitute
the red blood cells because they must go through full development
before they are functional. Blood loss greatly compromises the
performance of endurance athletes by reducing oxygen delivery
capacity.
Red blood cells transport oxygen, which is primarily bound to
hemoglobin. Hemoglobin is composed of a protein (globin) and a
pigment (heme). Heme contains iron, which binds oxygen. Each red
blood cell contains approximately 250 million hemoglobin molecules,
each able to bind four oxygen molecules—so each red blood cell can
bind up to a billion molecules of oxygen! There is an average of 15 g
of hemoglobin per 100 ml of whole blood. Each gram of hemoglobin
can combine with 1.33 ml of oxygen, so as much as 20 ml of oxygen
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can be bound for each 100 ml of blood. Therefore, when arterial
blood is saturated with oxygen, it has an oxygen-carrying capacity of
20 ml of oxygen per 100 ml of blood.
Blood Viscosity
Viscosity refers to the thickness of the blood. Recall from our
discussion of vascular resistance that the more viscous a fluid, the
more resistant it is to flow. Syrup is more viscous than water and
thus flows more slowly when poured. The viscosity of blood is
normally about twice that of water and increases as hematocrit
increases.
Because of oxygen transport by the red blood cells, an increase in
their number would be expected to maximize oxygen transport. But if
an increase in red blood cell count is not accompanied by a similar
increase in plasma volume, blood viscosity and vascular resistance
will increase, which could result in reduced blood flow. This generally
is not a problem unless the hematocrit reaches 60% or more.
Conversely, the combination of a low hematocrit with a high
plasma volume, which decreases the blood’s viscosity, appears to
have certain benefits for the blood’s transport function because the
blood can flow more easily. Unfortunately, a low hematocrit
frequently results from a reduced red blood cell count, as in diseases
such as anemia. Under these circumstances, the blood can flow
easily, but it contains fewer carriers, so oxygen transport is impeded.
For optimal physical performance, a low-normal hematocrit with a
normal or slightly elevated number of red blood cells is desirable.
This combination facilitates oxygen transport. Many endurance
athletes achieve this combination as part of their cardiovascular
system’s normal adaptation to training. This adaptation is discussed
in chapter 11.
In Review
Blood is about 55% to 60% plasma and 40% to 45% formed elements. Red
blood cells compose about 99% of the formed elements.
The hematocrit is the ratio of the formed elements in the blood (red cells, white
cells, and platelets) to the total blood volume. An average hematocrit for adult
men is 42% and for adult women is 38%.
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Oxygen is transported primarily by binding to the hemoglobin in red blood cells.
During endurance training, athletes respond with both a higher red cell volume
(RCV) and an expanded plasma volume (PV). Since the PV increase is higher
than the RCV increase, the hematocrit in these athletes tends to be somewhat
lower than that of sedentary individuals.
As blood viscosity increases, so does resistance to flow. Increasing the number
of red blood cells is advantageous to aerobic performance but only up to the
point (a hematocrit approaching 60%) where viscosity limits flow.
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IN CLOSING
In this chapter, we reviewed the structure and function of the cardiovascular
system. We learned how blood flow and blood pressure are regulated to meet
the body’s needs and explored the role of the cardiovascular system in
transporting and delivering oxygen and nutrients to the body’s cells while
clearing away metabolic wastes, including carbon dioxide. Knowing how
substances are moved within the body, we now look more closely at the
transport of oxygen and carbon dioxide. In the next chapter, we explore the role
of the respiratory system in delivering oxygen to, and removing carbon dioxide
from, the cells of the body.
KEY TERMS
arteries
arterioles
atherosclerosis
atrioventricular (AV) node
baroreceptor
bradycardia
capillaries
cardiac cycle
cardiac output ( )
chemoreceptor
diastolic blood pressure (DBP)
ejection fraction (EF)
electrocardiogram (ECG)
electrocardiograph
end-diastolic volume (EDV)
end-systolic volume (ESV)
extrinsic neural control
functional sympatholysis
heart murmur
hematocrit
hematopoiesis
hemoglobin
intercalated disks
mean arterial pressure (MAP)
mechanoreceptors
muscle pump
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myocardium
pericardium
premature ventricular contraction (PVC)
Purkinje fibers
sinoatrial (SA) node
stroke volume (SV)
systolic blood pressure (SBP)
tachycardia
vasoconstriction
vasodilation
veins
ventricular fibrillation
ventricular tachycardia
venules
STUDY QUESTIONS
1.
Describe the structure of the heart, the pattern of blood flow through the
valves and chambers of the heart, how the heart as a muscle is supplied
with blood, and what happens when the resting heart must suddenly
supply an exercising body.
2.
What events take place that allow the heart to contract, and how is heart
rate controlled?
3.
What is torsional contraction of the heart, and why is it important during
exercise?
4.
What is the difference between systole and diastole, and how do they
relate to SBP and DBP?
5.
6.
7.
What is the relationship between pressure, flow, and resistance?
8.
Describe the three important mechanisms for returning blood back to the
heart when someone is exercising in an upright position.
9.
Describe the primary functions of blood.
How is blood flow to the various regions of the body controlled?
How does muscle blood flow increase during exercise despite increased
sympathetic nerve activity that favors vasoconstriction?
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
400
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter
QUIZ tests your understanding of the material covered in the chapter.
401
402
7
The Respiratory System and Its
Regulation
In this chapter and in the web study guide
Pulmonary Ventilation
Inspiration
Expiration
ACTIVITY 7.1 Anatomy of the Respiratory System looks at the basic structures of the lung.
ACTIVITY 7.2 Inspiration and Expiration explores the key events of pulmonary ventilation.
Pulmonary Volumes
Pulmonary Diffusion
Blood Flow to the Lungs at Rest
Respiratory Membrane
Partial Pressures of Gases
Gas Exchange in the Alveoli
Summary of Pulmonary Gas Diffusion
AUDIO FOR FIGURE 7.4 describes the pressures in the pulmonary and systemic circulations.
ANIMATION FOR FIGURE 7.6 explains the varying partial pressures of oxygen and carbon dioxide in
the circulatory system.
AUDIO FOR FIGURE 7.7 describes the process of diffusion through a membrane.
AUDIO FOR FIGURE 7.9 describes the concept of the oxygen cascade.
Transport of Oxygen and Carbon Dioxide in the Blood
Oxygen Transport
Carbon Dioxide Transport
ANIMATION FOR FIGURE 7.10 breaks down the oxyhemoglobin dissociation curve and its effects in the
body.
Gas Exchange at the Muscles
403
Arterial–Venous Oxygen Difference
Oxygen Transport in the Muscle
Factors Influencing Oxygen Delivery and Uptake
Carbon Dioxide Removal
AUDIO FOR FIGURE 7.12 describes the arterial–mixed venous oxygen difference across muscle.
ACTIVITY 7.3 Arterial–Venous Oxygen Difference looks at differences in oxygen content in the blood of
resting and active people.
Regulation of Pulmonary Ventilation
ANIMATION FOR FIGURE 7.14 describes the factors involved in the regulation of breathing.
Afferent Feedback From Exercising Limbs
ACTIVITY 7.4 Regulation of Pulmonary Ventilation provides an in-depth review of the involuntary
regulation of pulmonary ventilation.
In Closing
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B
y any standard, Beijing, China, is one of the most polluted cities on the
planet. In preparation for the 2008 Olympic Games, nearly $17 billion was spent in
attempts to temporarily improve air quality, including cloud seeding to increase the
likelihood of rain showers in the region overnight. Factories were closed, traffic was
halted, and construction was put on hold for the duration of the Games. Yet air
pollution at the Olympics was still about two to four times higher than that of Los
Angeles on an average day, exceeding levels considered safe by the World Health
Organization. Several athletes opted out of events because of respiratory problems
or concerns, including Ethiopian marathon record holder Haile Gebrselassie and
2004 cycling silver medalist Sérgio Paulinho of Portugal. Athletes previously
diagnosed with asthma were allowed to use rescue inhalers. For the first time ever,
soccer matches were interrupted to give athletes time to recover from the pollutants,
smog, heat, and humidity. Athletes and spectators endured these conditions for a
few weeks, and there are no reports of long-term health problems among athletes or
spectators from exposure to the Beijing air. However, the residents of Beijing
encounter these adverse respiratory conditions on a daily basis.
The respiratory and cardiovascular systems combine to provide an
effective delivery system that carries oxygen to, and removes carbon
dioxide from, all tissues of the body.
This transportation involves four separate processes:
Pulmonary ventilation (breathing): movement of air into and
out of the lungs
Pulmonary diffusion: the exchange of oxygen and carbon
dioxide between the lungs and the blood
Transport of oxygen and carbon dioxide via the blood
Capillary diffusion: the exchange of oxygen and carbon
dioxide between the capillary blood and metabolically active
tissues
The first two processes are referred to as external respiration
because they involve moving gases from outside the body into the
lungs and then the blood. Once the gases are in the blood, they must
be transported to the tissues. When blood arrives at the tissues, the
fourth step of respiration occurs. This gas exchange between the
405
blood and the tissues is called internal respiration. Thus, external
and internal respiration are linked by the circulatory system. The
following sections examine all four components of respiration.
Pulmonary Ventilation
Pulmonary ventilation, or breathing, is the process by which we
move air into and out of the lungs. The anatomy of the respiratory
system is illustrated in figure 7.1. At rest, air is typically drawn into the
lungs through the nose, although the mouth must also be used when
the demand for air exceeds the amount that can comfortably be
brought in through the nose. Nasal breathing is advantageous
because the air is warmed and humidified as it swirls through the
bony irregular sinus surfaces (turbinates or conchae). Of equal
importance, the turbinates churn the inhaled air, causing dust and
other particles to contact and adhere to the nasal mucosa. This filters
out all but the tiniest particles, minimizing irritation and the threat of
respiratory infections. From the nose and mouth, the air travels
through the pharynx, larynx, trachea, and bronchial tree.
This transport zone also has physiological significance because it
comprises the so-called anatomical dead space. Because part of
each expired breath stays within this space, air from outside the body
mixes with this air with each inspiration, and the resulting mixture
reaches the alveoli.
These anatomical structures serve a transport function only,
because gas exchange does not occur in these structures. Exchange
of oxygen and carbon dioxide occurs when air finally reaches the
smallest respiratory units: the respiratory bronchioles and the alveoli.
The respiratory bronchioles are primarily transport tubes also but are
included in this region because they contain clusters of alveoli. This is
known as the respiratory zone because it is the site of gas exchange
in the lungs.
The lungs are not directly attached to the ribs. Rather, they are
suspended by the pleural sacs. The pleural sacs have a double wall:
the parietal pleura, which lines the thoracic wall, and the visceral or
pulmonary pleura, which lines the outer aspects of the lung. These
pleural walls envelop the lungs and have a thin film of fluid between
them that reduces friction during respiratory movements. In addition,
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these sacs are connected to the lungs and the inner surface of the
thoracic cage, causing the lungs to take the shape and size of the rib
or thoracic cage as the chest expands and contracts.
The anatomy of the lungs, the pleural sacs, the diaphragm muscle,
and the thoracic cage determines airflow into and out of the lungs,
that is, inspiration and expiration.
Inspiration
Inspiration is an active process involving the diaphragm and the
external intercostal muscles. Figure 7.2a shows the resting positions
of the diaphragm and the thoracic cage, or thorax. With inspiration,
the ribs and sternum are moved by the external intercostal muscles.
The ribs swing up and out and the sternum swings up and forward. At
the same time, the diaphragm contracts, flattening down toward the
abdomen.
FIGURE 7.1 (a) The anatomy of the respiratory system, illustrating the respiratory tract (i.e., nasal
cavity, pharynx, trachea, and bronchi). (b) The enlarged view of an alveolus shows the regions of gas
exchange between the alveolus and pulmonary blood in the capillaries.
These actions, illustrated in figure 7.2b, expand all three
dimensions of the thoracic cage, increasing the volume inside the
lungs. When the lungs are expanded they have a greater volume,
and the air within them has more space to fill. According to Boyle’s
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gas law, which states that pressure × volume is constant (at a
constant temperature), the pressure within the lungs decreases. As a
result, the pressure in the lungs (intrapulmonary pressure) is less
than the air pressure outside the body. Because the respiratory tract
is open to the outside, air rushes into the lungs to reduce this
pressure difference. This is how air moves into the lungs during
inspiration.
The pressure changes required for adequate ventilation at rest are
really quite small. For example, at the standard atmospheric pressure
at sea level (760 mmHg), inspiration may decrease the pressure in
the lungs (intrapulmonary pressure) by only about 2 to 3 mmHg.
However, during maximal respiratory effort, such as during exhaustive
exercise, the intrapulmonary pressure can decrease by 80 to 100
mmHg.
During forced or labored breathing, as during heavy exercise,
inspiration is further assisted by the action of other muscles, such as
the
scalenes
(anterior,
middle,
and
posterior)
and
sternocleidomastoid in the neck and the pectorals in the chest. These
muscles help raise the ribs even more than during regular breathing.
Expiration
At rest, expiration is a passive process involving relaxation of the
inspiratory muscles and elastic recoil of the lung tissue. As the
diaphragm relaxes, it returns to its normal upward, arched position.
As the external intercostal muscles relax, the ribs and sternum move
back into their resting positions (figure 7.2c). While this happens, the
elastic nature of the lung tissue causes it to recoil to its resting size.
This increases the pressure in the lungs and causes a proportional
decrease in volume in the thorax, and therefore air is forced out of the
lungs.
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FIGURE 7.2 The process of inspiration and expiration, showing (a) the positions of the ribs and thorax
at rest, and how movement of the ribs and diaphragm (b) increase the size of the thorax during
inspiration and (c) decrease the size of the thorax during expiration.
During forced breathing, expiration becomes a more active
process. The internal intercostal muscles actively pull the ribs down.
This action can be assisted by the latissimus dorsi and quadratus
lumborum muscles. Contracting the abdominal muscles increases the
intra-abdominal pressure, forcing the abdominal viscera upward
against the diaphragm and accelerating its return to the domed
position. These muscles also pull the rib cage down and inward.
The changes in intra-abdominal and intrathoracic pressure that
accompany forced breathing also help return venous blood back to
the heart, working together with the muscle pump in the legs to assist
the return of venous volume. As intra-abdominal and intrathoracic
pressure increases, it is transmitted to the great veins—the
pulmonary veins and superior and inferior venae cavae—that
transport blood back to the heart. When the pressure decreases, the
veins return to their original size and fill with blood. The changing
pressures within the abdomen and thorax squeeze the blood in the
veins, assisting its return through a milking action. This phenomenon
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is known as the respiratory pump and is essential in maintaining
adequate venous return.
Pulmonary Volumes
The volume of air in the lungs can be measured with a technique
called spirometry. A spirometer measures the volumes of air
inspired and expired and therefore changes in lung volume. Although
more sophisticated spirometers are used today, a simple spirometer
contains a bell filled with air that is partially submerged in water. A
tube runs from the subject’s mouth under the water and emerges
inside the bell, just above the water level. As the person exhales, air
flows down the tube and into the bell, causing the bell to rise. The bell
is attached to a pen, and its movement is recorded on a simple
rotating drum (figure 7.3).
This technique is used clinically to measure lung volumes,
capacities, and flow rates as an aid in diagnosing such respiratory
diseases as asthma, chronic obstructive pulmonary disease (COPD),
and emphysema.
The amount of air entering and leaving the lungs with each breath
is known as the tidal volume. The vital capacity (VC) is the greatest
amount of air that can be expired after a maximal inspiration. Even
after a full expiration, some air remains in the lungs. The amount of
air remaining in the lungs after a maximal expiration is the residual
volume (RV). The RV cannot be measured with spirometry. The total
lung capacity (TLC) is the sum of the VC and the RV.
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FIGURE 7.3 Lung volumes measured by spirometry.
In Review
Pulmonary ventilation (breathing) is the process by which air is moved into and
out of the lungs. It has two phases: inspiration and expiration.
Inspiration is an active process in which the diaphragm and the external
intercostal muscles contract, increasing the dimensions, and thus the volume, of
the thoracic cage. This decreases the pressure in the lungs, causing air to flow in.
Expiration at rest is normally a passive process. The inspiratory muscles and
diaphragm relax and the elastic tissue of the lungs recoils, returning the thoracic
cage to its smaller, normal dimensions. This increases the pressure in the lungs
and forces air out.
The pressure changes required for ventilation at rest are small, as little as 2
mmHg. However, during maximal respiratory effort, the intrapulmonary pressure
can decrease by 80 to 100 mmHg.
Forced or labored inspiration and expiration are active processes and involve
accessory muscle actions.
Breathing through the nose helps humidify and warm the air during inhalation and
filters out foreign particles from the air. Mouth breathing dominates at moderate to
high exercise intensities.
Lung volumes and capacities, along with rates of airflow into and out of the lungs,
are measured by spirometry.
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Pulmonary Diffusion
Gas exchange in the lungs between the alveoli and the capillary
blood, called pulmonary diffusion, serves two major functions:
It replenishes the blood’s oxygen supply, which is depleted at
the tissue level as it is used for oxidative energy production.
It removes carbon dioxide from venous blood returning from
systemic tissues.
Air is brought into the lungs during pulmonary ventilation, enabling
gas exchange to occur through pulmonary diffusion. Oxygen from the
air diffuses from the alveoli into the blood in the pulmonary capillaries,
and carbon dioxide diffuses from the blood into the alveoli in the
lungs. The alveoli are grapelike clusters, or air sacs, at the ends of
the terminal bronchioles.
RESEARCH PERSPECTIVE 7.1
Sprint Interval Training for Respiratory Muscles
Typical respiratory muscle endurance training (RMET) improves exercise
capacity and thus performance; such improvements are largely attributed to
reductions in the development of respiratory muscle fatigue. However, can a
shorter version of RMET based on the principle of high-intensity interval
training (respiratory muscle sprint-interval training, or RMSIT) elicit similar
improvements in respiratory muscle function?
A team of investigators recently sought to compare the effects of traditional
RMET versus RMSIT on respiratory muscle function.7 Mechanical airway
properties and respiratory muscle testing (e.g., respiratory muscle strength)
were measured before and after experimental sessions of RMET and RMSIT.
RMET consisted of continuous volitional hyperpnea (increased depth and rate
of breathing) performed for 30 min using a commercially available training
device. The RMSIT was a novel respiratory muscle training regimen
developed by the researchers. Using the same training device as with RMET,
the RMSIT regimen consisted of six short maximal respiratory sprints with
additional airway resistance to maximize respiratory muscle work. In this
fashion, RMSIT is characterized by higher respiratory muscle power output
and tension-time indices, but considerably lower total work compared to
RMET. The standard RMET and the novel RMSIT regimens reduced
respiratory muscle contractility to the same extent, triggering similar muscular
adaptations in response to training. Neither protocol altered mechanical airway
properties. Therefore, RMSIT appears to be a safe and time-saving alternative
to RMET.
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RMET can improve overall function for individuals who have undergone a
median sternotomy (splitting of the sternum to access underlying organs)
during cardiac surgery. Clinical exercise physiologists are interested in
exercise training adaptations that occur with structured cardiac rehabilitation
programs. The results of a 2013 study suggest that it would be beneficial to
include exercises that improve the strength of the inspiratory muscles as part
of a cardiac rehabilitation program.4 This type of training would reduce
inspiratory muscle effort and further improve ventilatory efficiency in patients
after open-heart surgery.
Blood from the body (except for that returning from the lungs)
returns through the vena cava to the right side of the heart. From the
right ventricle, this blood is pumped through the pulmonary artery to
the lungs, ultimately working its way into the pulmonary capillaries.
These capillaries form a dense network around the alveolar sacs and
are so small that the red blood cells must pass through them in single
file, such that the maximal surface area of each cell is exposed to the
surrounding lung tissue. This is where pulmonary diffusion occurs.
Blood Flow to the Lungs at Rest
At rest the lungs receive approximately 4 to 6 L/min of blood flow,
depending on body size. Because cardiac output from the right side
of the heart approximates cardiac output from the left side of the
heart, blood flow to the lungs matches blood flow to the systemic
circulation. However, pressure and vascular resistance in the blood
vessels in the lungs are different than in the system circulation. The
mean pressure in the pulmonary artery is ~15 mmHg (systolic
pressure is ~25 mmHg and diastolic pressure is ~8 mmHg) compared
to the mean pressure in the aorta of ~95 mmHg. The pressure in the
left atrium, where blood is returning to the heart from the lungs, is ~5
mmHg; thus, there is not a great pressure difference across the
pulmonary circulation (15 − 5 mmHg). Figure 7.4 illustrates the
differences in pressures between the pulmonary and systemic
circulation.
Recalling the discussion of blood flow in the cardiovascular system
from chapter 6, pressure = flow × resistance. Since blood flow to the
lungs is equal to that of the systemic circulation, and there is a
substantially lower change in pressure across the pulmonary vascular
system, resistance is proportionally lower compared to that in the
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systemic circulation. This is reflected in differences in the anatomy of
the vessels in the pulmonary versus systemic circulation: The
pulmonary blood vessels are thin walled, with relatively little smooth
muscle.
Respiratory Membrane
Gas exchange between the air in the alveoli and the blood in the
pulmonary capillaries occurs across the respiratory membrane (also
called the alveolar-capillary membrane). This membrane, depicted in
figure 7.5, is composed of
the alveolar wall,
the capillary wall, and
their respective basement membranes.
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FIGURE 7.4 Comparison of pressures (mmHg) in the pulmonary and systemic circulations.
The primary function of these membranous surfaces is for gas
exchange. The respiratory membrane is very thin, measuring only 0.5
to 4 mm. As a result, the gases in the nearly 300 million alveoli are in
close proximity to the blood circulating through the capillaries.
Partial Pressures of Gases
415
The air we breathe is a mixture of gases. Each exerts a pressure in
proportion to its concentration in the gas mixture. The individual
pressures from each gas in a mixture are referred to as partial
pressures. According to Dalton’s law, the total pressure of a mixture
of gases equals the sum of the partial pressures of the individual
gases in that mixture.
Consider the air we breathe. It is composed of 79.04% nitrogen
(N2), 20.93% oxygen (O2), and 0.03% carbon dioxide (CO2). These
percentages remain constant regardless of altitude. At sea level, the
atmospheric (or barometric) pressure is approximately 760 mmHg,
which is also referred to as standard atmospheric pressure. Thus, if
the total atmospheric pressure is 760 mmHg, then the partial
pressure of nitrogen (PN2) in air is 600.7 mmHg (79.04% of the total
760 mmHg pressure). Oxygen’s partial pressure (PO2) is 159.1
mmHg (20.93% of 760 mmHg), and carbon dioxide’s partial pressure
(PCO2) is 0.2 mmHg (0.03% of 760 mmHg).
In the human body, gases are usually dissolved in fluids, such as
blood plasma. According to Henry’s law, gases dissolve in liquids in
proportion to their partial pressures, depending also on their
solubilities in the specific fluids and on the temperature. A gas’s
solubility in blood is a constant, and blood temperature also remains
relatively constant at rest. Thus, the most critical factor for gas
exchange between the alveoli and the blood is the pressure gradient
between the gases in the two areas.
Gas Exchange in the Alveoli
Differences in the partial pressures of the gases in the alveoli and the
gases in the blood create a pressure gradient across the respiratory
membrane. This forms the basis of gas exchange during pulmonary
diffusion. If the pressures on each side of the membrane were equal,
the gases would be at equilibrium and would not move. But the
pressures are not equal, so gases move according to partial pressure
gradients.
Oxygen Exchange
The PO2 of air outside the body at standard atmospheric pressure is
159 mmHg. But this pressure decreases to about 105 mmHg when
air is inhaled and enters the alveoli, where it is moistened and mixes
416
with the air in the alveoli. The alveolar air is saturated with water
vapor (which has its own partial pressure) and contains more carbon
dioxide than the inspired air. Both the increased water vapor pressure
and increased partial pressure of carbon dioxide contribute to the
total pressure in the alveoli. Fresh air that ventilates the lungs is
constantly mixed with the air in the alveoli while some of the alveolar
gases are exhaled to the environment. As a result, alveolar gas
concentrations remain relatively stable.
The blood, stripped of much of its oxygen by the metabolic needs
of the tissues, typically enters the pulmonary capillaries with a PO2 of
about 40 mmHg (see figure 7.6). This is about 60 to 65 mmHg less
than the PO2 in the alveoli. In other words, the pressure gradient for
oxygen across the respiratory membrane is typically about 65 mmHg.
As noted earlier, this pressure gradient drives the oxygen from the
alveoli into the blood to equilibrate the pressure of the oxygen on
each side of the membrane.
FIGURE 7.5 The anatomy of the respiratory membrane, showing the exchange of oxygen and carbon
dioxide between an alveolus and pulmonary capillary blood.
RESEARCH PERSPECTIVE 7.2
Exercise Training Offsets Decreases in Lung Diffusing
Capacity with Aging
The structure and function of the pulmonary vasculature contributes to
maximal aerobic capacity ( O2max), such that a larger, more distensible
vascular network in the lungs is associated with greater aerobic exercise
capacity. During exercise, increased cardiac output and pulmonary perfusion
pressure cause an expansion of the highly compliant pulmonary capillary
417
network, resulting in increased lung diffusing capacity, alveolar-capillary
membrane conductance, and pulmonary capillary blood volume.
As we age, the structure and function of the pulmonary circulation
changes, resulting in increased pulmonary vascular stiffness, pulmonary
vascular pressures, and pulmonary vascular resistance, all of which impair
recruitment and distension of pulmonary capillaries during exercise. However,
these age-related alterations do not appear to limit the expansion of
pulmonary capillaries during exercise in healthy older adults. The pulmonary
vascular response to exercise in endurance-trained, highly fit older adults is
not well defined. It is plausible that a higher O2max may cause the demand
for cardiac output and pulmonary blood flow during exercise to remain
elevated in older athletes, thus predisposing highly fit older adults to
impairments in pulmonary vascular expansion and pulmonary gas exchange
relative to the metabolic demands of exercise.
This concept was recently tested by a group of investigators who
characterized lung diffusing capacity, alveolar-capillary membrane
conductance, and pulmonary capillary blood volume in response to
incremental exhaustive exercise in aerobically trained older adults.3 The
authors hypothesized that older athletes would be limited in their ability to
expand the pulmonary vascular network during high-intensity exercise. Their
findings confirmed the negative age-related reductions in lung diffusing
capacity, alveolar-capillary membrane conductance, and pulmonary capillary
blood volume during exercise; however, these variables were increased in
exercise-trained older adults during exercise relative to age-matched,
nontrained individuals. In contrast to the original hypothesis, there was a
progressive increase in lung diffusing capacity throughout exercise in
exercise-trained adults, suggesting that the expansion of the pulmonary
capillary network during exercise is not limited during exercise in highly fit
older adults. Follow-up studies should include measures of pulmonary
vascular pressures to more specifically determine the relation between
increases in lung diffusing capacity and the pulmonary vascular response to
exercise.
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FIGURE 7.6 Partial pressure of oxygen (PO2) and carbon dioxide (PCO2) in blood as a result of gas
exchange in the lungs and gas exchange between the capillary blood and tissues.
The PO2 in the alveoli stays relatively constant at about 105
mmHg. As the deoxygenated blood enters the pulmonary artery, the
PO2 in the blood is only about 40 mmHg. But as the blood moves
along the pulmonary capillaries, gas exchange occurs. By the time
the pulmonary blood reaches the venous end of these capillaries, the
PO2 in the blood equals that in the alveoli (approximately 105 mmHg),
and the blood is now considered to be saturated with oxygen at its full
carrying capacity. The blood leaving the lungs through the pulmonary
veins and subsequently returning to the systemic (left) side of the
heart has a rich supply of oxygen to deliver to the tissues. Notice,
419
however, that the PO2 in the pulmonary vein is 100 mmHg, not the
105 mmHg found in the alveolar air and pulmonary capillaries. This
difference is attributable to the fact that about 2% of the blood is
shunted from the aorta directly to the lung to meet the oxygen needs
of the lung itself. This blood has a lower PO2 and reenters the
pulmonary vein along with fully saturated blood returning to the left
atrium that has just completed gas exchange. This blood mixes and
thus decreases the PO2 of the blood returning to the heart.
Diffusion through tissues is described by Fick’s law (figure 7.7).
Fick’s law states that the rate of diffusion through a tissue such as the
respiratory membrane is proportional to the surface area and the
difference in the partial pressure of gas between the two sides of the
tissue. For example, the greater the pressure gradient for oxygen is
across the respiratory membrane, the more rapidly oxygen diffuses
across it. The rate of diffusion is also inversely proportional to the
thickness of the tissue in which the gas must diffuse. Additionally, the
diffusion constant, which is unique to each gas, influences the rate of
diffusion across the tissue. Carbon dioxide has a much lower diffusion
constant than oxygen; therefore, even though there is not as great a
difference between alveolar and capillary partial pressure of carbon
dioxide as there is for oxygen, carbon dioxide still diffuses easily.
The rate at which oxygen diffuses from the alveoli into the blood is
referred to as the oxygen diffusion capacity and is expressed as
the volume of oxygen that diffuses through the membrane each
minute for a pressure difference of 1 mmHg. At rest, the oxygen
diffusion capacity is about 21 ml of oxygen per minute per 1 mmHg of
pressure difference between the alveoli and the pulmonary capillary
blood. Although the partial pressure gradient between venous blood
coming into the lung and the alveolar air is about 65 mmHg (105
mmHg − 40 mmHg), the oxygen diffusion capacity is calculated on
the basis of the mean pressure in the pulmonary capillary, which has
a substantially higher PO2. The gradient between the mean partial
pressure of the pulmonary capillary and the alveolar air is
approximately 11 mmHg, which would provide a diffusion of 231 ml of
oxygen per minute through the respiratory membrane. During
maximal exercise, the oxygen diffusion capacity may increase by up
to three times the resting rate, because blood is returning to the lungs
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severely desaturated and thus there is a greater partial pressure
gradient from the alveoli to the blood. In fact, rates of more than 80
ml/min have been observed among highly trained athletes.
FIGURE 7.7 Diffusion through a sheet of tissue. The amount of gas (
gas)
transferred is proportional to
the area (A), a diffusion constant (D), and the difference in partial pressure (P1 − P2) and is inversely
proportional to the thickness (T). The constant is proportional to the gas solubility (Sol) but inversely
proportional to the square root of its molecular weight (MW).
The increase in oxygen diffusion capacity from rest to exercise is
caused by a relatively inefficient, sluggish circulation through the
lungs at rest, which results primarily from limited perfusion of the
upper regions of the lungs attributable to gravity. If the lung is divided
into three zones as depicted in figure 7.8, at rest only the bottom third
(zone 3) of the lung is perfused with blood. During exercise, however,
blood flow through the lungs is greater, primarily as a result of
elevated blood pressure, which increases lung perfusion.
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FIGURE 7.8 Explanation of the uneven distribution of blood flow in the lung.
Carbon Dioxide Exchange
Carbon dioxide, like oxygen, moves along a partial pressure gradient.
As shown in figure 7.6, the blood passing from the right side of the
heart through the alveoli has a PCO2 of about 46 mmHg. Air in the
alveoli has a PCO2 of about 40 mmHg. Although this results in a
relatively small pressure gradient of only about 6 mmHg, it is more
than adequate to allow for exchange of CO2. Carbon dioxide’s
diffusion coefficient is 20 times greater than that of oxygen, so CO2
can diffuse across the respiratory membrane much more rapidly.
Summary of Pulmonary Gas Diffusion
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The partial pressures of gases involved in pulmonary diffusion are
summarized in table 7.1. Note that the total pressure in the venous
blood is only 706 mmHg, 54 mmHg lower than the total pressure in
dry air and alveolar air. This is the result of a much greater decrease
in PO2 compared with the increase in PCO2 as the blood goes
through the body’s tissues.
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FIGURE 7.9 The oxygen cascade depicts the dropping partial pressures of oxygen (in this depiction, at
sea level) from dry ambient air to the tissues and into the venous circulation draining those tissues.
Figure 7.9 shows the dropping partial pressures of oxygen at sea
level from dry ambient air to the tissues and into the venous
circulation draining those tissues. This is referred to as the oxygen
cascade. At a sea level barometric pressure (PB) of 760 mmHg, PO2
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in the ambient air (if it were completely devoid of moisture, which
does not occur in nature) would be
0.2093 × 760 mmHg = 159 mmHg.
As dry air moves through the nose and mouth and becomes
humidified water vapor (which has a partial pressure, PH2O, of 47
mmHg at body temperature), air in the trachea has a partial pressure
of
0.2093 × (760 – 47) = 149 mmHg.
In the alveoli, air now becomes a mixture combining PCO2 in blood
returning from the systemic circulation and PO2 from the tracheal air
and equilibrates at approximately 105 mmHg. As oxygen diffuses
from the alveoli into the pulmonary capillaries and into arterial blood,
PO2 continues to drop slightly down diffusion gradients, since
pulmonary capillary blood is a mixture of arterial and venous blood, a
so-called admixture.
At the tissue (e.g., muscle) level, cells extract O2 from the arterial
supply for aerobic metabolism, and the drop in PO2 from arterial
blood to venous blood flowing away from the tissues represents the
arterial–venous oxygen difference, or (a-v)O2 difference. Note that the
PO2 at the mitochondrial level is extremely low, approximately 1 to 2
mmHg. This ensures optimal O2 delivery to these organelles, the
ultimate destination of oxygen where it is used in oxidative
phosphorylation.
In Review
Pulmonary diffusion is the process by which gases are exchanged across the
respiratory membrane in the alveoli.
Dalton’s law states that the total pressure of a mixture of gases equals the sum of
the partial pressures of the individual gases in that mixture.
The amount and rate of gas exchange that occur across the membrane depend
primarily on the partial pressure of each gas, although other factors are also
important, as shown by Fick’s law. Gases diffuse along a pressure gradient,
moving from an area of higher pressure to one of lower pressure. Thus, oxygen
enters the blood and carbon dioxide leaves it.
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Oxygen diffusion capacity increases as one moves from rest to exercise. When
exercising muscles require more oxygen to be used in the metabolic processes,
venous oxygen is depleted and oxygen exchange at the alveoli is facilitated.
The pressure gradient for carbon dioxide exchange is less than for oxygen
exchange, but carbon dioxide’s diffusion coefficient is 20 times greater than that of
oxygen, so carbon dioxide crosses the membrane readily without a large pressure
gradient.
Transport of Oxygen and Carbon Dioxide in the
Blood
We have considered how air moves into and out of the lungs via
pulmonary ventilation and how gas exchange occurs via pulmonary
diffusion. Next we consider how gases are transported in the blood to
deliver oxygen to the tissues and remove the carbon dioxide that the
tissues produce.
Oxygen Transport
Oxygen is transported by the blood either (1) combined with
hemoglobin in the red blood cells (greater than 98%) or (2) dissolved
in the blood plasma (less than 2%). Only about 3 ml of oxygen is
dissolved in each liter of plasma. Assuming a total plasma volume of
3 to 5 L, only about 9 to 15 ml of oxygen can be carried in the
dissolved state. This limited amount of oxygen cannot adequately
meet the needs of even resting body tissues, which generally require
more than 250 ml of oxygen per minute (depending on body size).
However, hemoglobin, a protein contained within each of the body’s 4
to 6 billion red blood cells, allows the blood to transport nearly 70
times more oxygen than can be dissolved in plasma.
Hemoglobin Saturation
As just noted, over 98% of oxygen is transported in the blood bound
to hemoglobin. Each molecule of hemoglobin can carry four
molecules of oxygen. When oxygen binds to hemoglobin, it forms
oxyhemoglobin; hemoglobin that is not bound to oxygen is referred to
as deoxyhemoglobin. The binding of oxygen to hemoglobin depends
on the PO2 in the blood and the bonding strength, or affinity, between
hemoglobin and oxygen. The curve in figure 7.10 is an oxygen–
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hemoglobin dissociation curve, which shows the amount of
hemoglobin saturated with oxygen at different PO2 values. The shape
of the curve is extremely important for its function in the body. The
relatively flat upper portion means that at high PO2 concentrations,
such as in the lungs, large drops in PO2 result in only small changes
in hemoglobin saturation. This is called the “loading” portion of the
curve. A high blood PO2 results in almost complete hemoglobin
saturation, which means that the maximal amount of oxygen is
bound. But as the PO2 decreases, so does hemoglobin saturation.
The steep portion of the curve coincides with PO2 values typically
found in the tissues of the body. Here, relatively small changes in PO2
result in large changes in saturation. This is advantageous because
this is the “unloading” portion of the curve where hemoglobin loses its
oxygen to the tissues.
Many factors determine the hemoglobin saturation. If, for example,
the blood becomes more acidic, the dissociation curve shifts to the
right. This indicates that more oxygen is being unloaded from the
hemoglobin at the tissue level. This rightward shift of the curve (see
figure 7.11a), attributable to a decline in pH, is referred to as the Bohr
effect. The pH in the lungs is generally high, so hemoglobin passing
through the lungs has a strong affinity for oxygen, encouraging high
saturation. At the tissue level, especially during exercise, the pH is
lower, causing oxygen to dissociate from hemoglobin, thereby
supplying oxygen to the tissues. With exercise, the ability to unload
oxygen to the muscles increases as the muscle pH decreases.
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FIGURE 7.10 Oxyhemoglobin dissociation curve.
FIGURE 7.11 The effects of (a) changing blood pH and (b) blood temperature on the oxyhemoglobin
dissociation curve.
Blood temperature also affects oxygen dissociation. As shown in
figure 7.11b, increased blood temperature shifts the dissociation
curve to the right, indicating that oxygen is unloaded from hemoglobin
more readily at higher temperatures. Because of this, the hemoglobin
unloads more oxygen when blood circulates through the metabolically
heated active muscles.
Blood Oxygen-Carrying Capacity
The oxygen-carrying capacity of blood is the maximal amount of
oxygen the blood can transport. It depends primarily on the blood
hemoglobin content. Each 100 ml of blood contains an average of 14
to 18 g of hemoglobin in men and 12 to 16 g in women. Each gram of
hemoglobin can combine with about 1.34 ml of oxygen, so the
oxygen-carrying capacity of blood is approximately 16 to 24 ml per
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100 ml of blood when blood is fully saturated with oxygen. At rest, as
the blood passes through the lungs, it is in contact with the alveolar
air for approximately 0.75 s. This is sufficient time for hemoglobin to
become 98% to 99% saturated. At high intensities of exercise, the
contact time is greatly reduced, which can reduce the binding of
hemoglobin to oxygen and slightly decrease the saturation, although
the unique “S” shape of the curve guards against large drops.
People with low hemoglobin concentrations, such as those with
anemia, have reduced oxygen-carrying capacities. Depending on the
severity of the condition, these people might feel few effects of
anemia while they are at rest because their cardiovascular system
can compensate for reduced blood oxygen content by increasing
cardiac output. However, during activities in which oxygen delivery
can become a limitation, such as highly intense aerobic effort,
reduced blood oxygen content limits performance.
Carbon Dioxide Transport
Carbon dioxide also relies on the blood for transportation. Once
carbon dioxide is released from the cells, it is carried in the blood
primarily in three forms:
As bicarbonate ions resulting from the dissociation of carbonic
acid
Dissolved in plasma
Bound to hemoglobin (called carbaminohemoglobin)
Bicarbonate Ion
The majority of carbon dioxide is carried in the form of bicarbonate
ion. Bicarbonate accounts for the transport of 60% to 70% of the
carbon dioxide in the blood. Carbon dioxide and water molecules
combine to form carbonic acid (H2CO3). This reaction is catalyzed by
the enzyme carbonic anhydrase, which is found in red blood cells.
Carbonic acid is unstable and quickly dissociates, freeing a hydrogen
ion (H+) and forming a bicarbonate ion (HCO3−):
CO2 + H2O → H2CO3 → H+ + HCO3−
The H+ subsequently binds to hemoglobin, and this binding triggers
the Bohr effect, mentioned previously, which shifts the oxygen–
hemoglobin dissociation curve to the right. The bicarbonate ion
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diffuses out of the red blood cell and into the plasma. In order to
prevent electrical imbalance from the shift of the negatively charged
bicarbonate ion into the plasma, a chloride ion diffuses from the
plasma into the red blood cell. This is called the chloride shift.
Additionally, the formation of hydrogen ions through this reaction
enhances oxygen unloading at the level of the tissue. Through this
mechanism, hemoglobin acts as a buffer, binding and neutralizing the
H+ and thus preventing any significant acidification of the blood. Acid–
base balance is discussed in more detail in chapter 8.
When the blood enters the lungs, where the PCO2 is lower, the H+
and bicarbonate ions rejoin to form carbonic acid, which then
dissociates into carbon dioxide and water:
H+ + HCO3− → H2CO3 → CO2 + H2O
The carbon dioxide that is thus re-formed can enter the alveoli and be
exhaled.
Dissolved Carbon Dioxide
Part of the carbon dioxide released from the tissues is dissolved in
plasma, but only a small amount, typically just 7% to 10%, is
transported this way. This dissolved carbon dioxide comes out of
solution where the PCO2 is low, as in the lungs. There it diffuses from
the pulmonary capillaries into the alveoli to be exhaled.
Carbaminohemoglobin
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Carbon dioxide transport also can occur when the gas binds with
hemoglobin, forming carbaminohemoglobin. The compound is so
named because carbon dioxide binds with amino acids in the globin
part of the hemoglobin molecule, rather than with the heme group as
oxygen does. Because carbon dioxide binding occurs on a different
part of the hemoglobin molecule than does oxygen binding, the two
processes do not compete. However, carbon dioxide binding varies
with the oxygenation of the hemoglobin (deoxyhemoglobin binds
carbon dioxide more easily than oxyhemoglobin) and the partial
pressure of CO2. Carbon dioxide is released from hemoglobin when
PCO2 is low, as it is in the lungs. Thus, carbon dioxide is readily
released from the hemoglobin in the lungs, allowing it to enter the
alveoli to be exhaled.
In Review
Oxygen is transported in the blood primarily bound to hemoglobin (as
oxyhemoglobin), although a small part of it is dissolved in plasma.
To better respond to increased oxygen demand, hemoglobin unloading of oxygen
(desaturation) is enhanced (i.e., the curve shifts to the right) when
PO2 decreases,
pH decreases, or
temperature increases.
Because of the sigmoid shape of the curve, loading of hemoglobin with oxygen in
the lungs is only minimally affected by the shift.
In the arteries, hemoglobin is usually about 98% saturated with oxygen. This is a
higher oxygen content than our bodies require, so the blood’s oxygen-carrying
capacity seldom limits performance in healthy individuals.
Carbon dioxide is transported in the blood primarily as bicarbonate ion. This
prevents the formation of carbonic acid, which can cause H+ to accumulate and
lower the pH. Smaller amounts of carbon dioxide are either dissolved in the
plasma or bound to hemoglobin.
Gas Exchange at the Muscles
We have considered how the respiratory and cardiovascular systems
bring air into our lungs, exchange oxygen and carbon dioxide in the
alveoli, and transport oxygen to the muscles and carbon dioxide to
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the lungs. We now consider the delivery of oxygen from the capillary
blood to the muscle tissue.
FIGURE 7.12 The arterial–mixed venous oxygen difference, or (a- )O2 difference, across the muscle
(a) at rest and (b) during intense aerobic exercise.
Arterial–Venous Oxygen Difference
At rest, the oxygen content of arterial blood is about 20 ml of oxygen
per 100 ml of blood. As shown in figure 7.12a, this value decreases to
15 to 16 ml of oxygen per 100 ml after the blood has passed through
the capillaries into the venous system. This difference in oxygen
content between arterial and venous blood is referred to as the
arterial–mixed venous oxygen difference, or (a- )O2 difference.
The term mixed venous ( ) refers to the oxygen content of blood in
the right atrium, which comes from all parts of the body, both active
and inactive. The difference between arterial and mixed venous
oxygen content reflects the 4 to 5 ml of oxygen per 100 ml of blood
taken up by the tissues. The amount of oxygen taken up is
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proportional to its use for oxidative energy production. Thus, as the
rate of oxygen use increases, the (a- )O2 difference also increases. It
can increase to 15 to 16 ml per 100 ml of blood during maximal levels
of endurance exercise (figure 7.12b). However, at the level of the
contracting muscle, the arterial– venous oxygen difference, or (av)O2 difference, during intense exercise can increase to 17 to 18 ml
per 100 ml of blood. Note that there is not a bar over the v in this
instance because we are now looking at local muscle venous blood,
not mixed venous blood in the right atrium. During intense exercise,
more oxygen is unloaded to the active muscles because the PO2 in
the muscles is substantially lower than in arterial blood.
Oxygen Transport in the Muscle
Before oxygen can be used in oxidative metabolism, it must be
transported in the muscle to the mitochondria by a molecule called
myoglobin. Myoglobin is similar in structure to hemoglobin, but
myoglobin has a much greater affinity for oxygen than hemoglobin.
This concept is illustrated in figure 7.13. At PO2 values less than 20
mmHg, the myoglobin dissociation curve is much steeper than the
dissociation curve for hemoglobin. Myoglobin releases its oxygen
content only under conditions in which the PO2 is very low. Note from
figure 7.13 that at a PO2 at which venous blood is unloading oxygen,
myoglobin is loading oxygen. It is estimated that the PO2 in the
mitochondria of an exercising muscle may be as low as 1 mmHg;
thus, myoglobin readily delivers oxygen to the mitochondria.
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FIGURE 7.13 A comparison of the dissociation curves for myoglobin and hemoglobin.
Factors Influencing Oxygen Delivery and Uptake
The rates of oxygen delivery and uptake depend on three major
variables:
Oxygen content of blood
Blood flow
Local conditions (e.g., pH, temperature)
With exercise, each of these variables is adjusted to ensure
increased oxygen delivery to active muscle. Under normal
circumstances, hemoglobin is about 98% saturated with oxygen. Any
reduction in the blood’s normal oxygen-carrying capacity would hinder
oxygen delivery and reduce cellular uptake of oxygen. Likewise, a
reduction in the PO2 of the arterial blood would lower the partial
pressure gradient, limiting the unloading of oxygen at the tissue level.
Exercise increases blood flow through the muscles. As more blood
carries oxygen through the muscles, less oxygen must be removed
from each 100 ml of blood (assuming the demand is unchanged).
Thus, increased blood flow improves oxygen delivery.
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Many local changes in the muscle during exercise affect oxygen
delivery and uptake. For example, muscle activity increases muscle
acidity because of lactate production. Also, muscle temperature and
carbon dioxide concentration both increase because of increased
metabolism. All these changes increase oxygen unloading from the
hemoglobin molecule, facilitating oxygen delivery and uptake by the
muscles.
Carbon Dioxide Removal
Carbon dioxide exits the cells by simple diffusion in response to the
partial pressure gradient between the tissue and the capillary blood.
For example, muscles generate carbon dioxide through oxidative
metabolism, so the PCO2 in muscles is relatively high compared with
that in the capillary blood. Consequently, CO2 diffuses out of the
muscles and into the blood to be transported to the lungs.
In Review
The (a- )O2 difference is the difference in the oxygen content of arterial and
mixed venous blood throughout the body. This measure reflects the amount of
oxygen taken up by the tissues, active and inactive.
The (a- )O2 difference increases from a resting value of about 4 to 5 ml per 100
ml of blood up to values of 18 ml per 100 ml of blood during intense exercise. This
increase reflects an increased extraction of oxygen from arterial blood by active
muscle, thus decreasing the oxygen content of the venous blood.
Oxygen delivery to the tissues depends on the oxygen content of the blood, blood
flow to the tissues, and local conditions (e.g., tissue temperature and PO2).
Within muscle, oxygen is transported to the mitochondria by a molecule called
myoglobin. Compared to the oxyhemoglobin dissociation curve, the myoglobin-O2
dissociation curve is much steeper at low PO2 values.
Myoglobin releases its oxygen only at a very low PO2. This is compatible with the
PO2 found in exercising muscle, which may be as low as 1 mmHg.
Carbon dioxide exchange at the tissues is similar to oxygen exchange, except that
carbon dioxide leaves the muscles, where it is formed, and enters the blood to be
transported to the lungs for clearance.
Regulation of Pulmonary Ventilation
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Maintaining homeostatic balance in blood PO2, PCO2, and pH
requires a high degree of coordination between the respiratory,
muscular, and circulatory systems. Much of this coordination is
accomplished by involuntary regulation of pulmonary ventilation. This
control is not yet fully understood, although many of the intricate
neural controls have been identified.
The respiratory muscles are under the direct control of motor
neurons, which are in turn regulated by respiratory centers
(inspiratory and expiratory) located within the brain stem (in the
medulla oblongata and pons). These centers establish the rate and
depth of breathing by sending out periodic impulses to the respiratory
muscles. The cortex can override these centers if voluntary control of
respiration is desired. Additionally, input from other parts of the brain
occurs under certain conditions.
The inspiratory area of the brain (dorsal respiratory group) contains
cells that intrinsically fire and control the basic rhythm of ventilation.
The expiratory area is quiet during normal breathing (recall that
expiration is a passive process at rest). However, during forceful
breathing such as during exercise, the expiratory area actively sends
signals to the muscles of expiration. Two other brain centers aid in
the control of respiration. The apneustic area has an excitatory effect
on the inspiratory center, resulting in prolonged firing of the
inspiratory neurons. Finally, the pneumotaxic center inhibits or
switches off inspiration, helping to regulate inspiratory volume.
RESEARCH PERSPECTIVE 7.3
Ventilation During Exercise in Asthma
Asthma, a condition in which the airways are inflamed and narrowed, changes
airway function and makes breathing difficult. Because these changes in
airway function are variable, asthmatics experience daily fluctuations in airway
inflammation, airway hyper-responsiveness, pulmonary function, and clinical
symptoms. Regular aerobic exercise is recommended for asthmatics, and
asthmatics who are physically active show improvements in exercise capacity.
However, despite a large body of literature characterizing exercise-induced
bronchoconstriction in asthmatics, a significant gap in knowledge exists with
regard to the influences of variable airway function at rest on the responses to
aerobic exercise.
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A recent study sought to determine the effects of both improved and
worsened preexercise airway mechanical function on the ventilatory
responses to aerobic exercise in asthmatic and nonasthmatic adults.5 All
subjects completed four separate exercise bouts of 3 min of cycling at 70% of
their peak workload, followed by continuous exercise at 85% of peak workload
until volitional exhaustion. Each exercise bout was preceded by one of four
different interventions: (1) inhalation of a fast-acting 2-agonist to improve
airway function, (2) a eucapnic voluntary hyperpnea challenge to worsen
airway function, (3) a sham version of the hyperpnea, and (4) a control trial.
Pulmonary function was assessed using an automated spirometer.
Surprisingly, despite markedly different preexercise pulmonary function
(experimentally manipulated by each intervention) in asthmatic adults,
exercise ventilation was nearly identical among the four conditions. Moreover,
there were no differences in exercise ventilation between asthmatic and
nonasthmatic adults during any of the four different interventions. These data
demonstrate that the pulmonary system of asthmatic adults is capable of
adequately responding to the acute demand for increased airflow necessitated
by high-intensity aerobic exercise. Clinically, the findings of this study support
the notion that habitual aerobic exercise is beneficial for adults with asthma.
The respiratory centers do not act alone in controlling breathing.
Breathing also is regulated and modified by the changing chemical
environment in the body. For example, sensitive areas in the brain
respond to changes in carbon dioxide and H+ levels. The central
chemoreceptors in the brain are stimulated by an increase in H+ ions
in the cerebrospinal fluid. The blood–brain barrier is relatively
impermeable to H+ ions or bicarbonate. However, CO2 readily diffuses
across the blood–brain barrier and then reacts to increase H+ ions.
This, in turn, stimulates the inspiratory center, which then activates
the neural circuitry to increase the rate and depth of respiration. This
increase in respiration, in turn, increases the removal of carbon
dioxide and H+.
Chemoreceptors in the aortic arch (the aortic bodies) and in the
bifurcation of the common carotid artery (the carotid bodies) not only
are sensitive primarily to blood changes in PO2 but also respond to
changes in H+ concentration and PCO2. The carotid chemoreceptors
are more sensitive to changes in H+ concentrations and PCO2.
Overall, PCO2 appears to be the strongest stimulus for the regulation
of breathing. When carbon dioxide levels become too high, carbonic
acid forms, then quickly dissociates, giving off H+. If H+ accumulates,
437
the blood becomes too acidic (pH decreases). Thus, an increased
PCO2 stimulates the inspiratory center to increase respiration—not to
bring in more oxygen but to rid the body of excess carbon dioxide and
limit further pH changes.
In addition to the chemoreceptors, other neural mechanisms
influence breathing. The pleurae, bronchioles, and alveoli in the lungs
contain stretch receptors. When these areas are excessively
stretched, that information is relayed to the expiratory center. The
expiratory center responds by shortening the duration of an
inspiration, which decreases the risk of overinflating the respiratory
structures. This response is known as the Hering-Breuer reflex.
Many control mechanisms are involved in the regulation of
breathing, as shown in figure 7.14. Such simple stimuli as emotional
distress or an abrupt change in the temperature of the surroundings
can affect breathing. But all these control mechanisms are essential.
The goal of respiration is to maintain appropriate levels of the blood
and tissue gases as well as proper pH for normal cellular function.
Small changes in any of these, if not carefully controlled, could impair
physical activity and jeopardize health.
Afferent Feedback From Exercising Limbs
The respiratory system responds almost immediately to increased
ventilation at the initiation of exercise, even before there is a
significant increase in the metabolic demand from exercising muscle.
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The fast initiation of the drive to breathe results from a combination of
central command (the brain’s feedforward mechanism) and afferent
neural feedback from the working limbs.
FIGURE 7.14 An overview of the processes involved in respiratory regulation.
In addition to those physiological mechanisms, it has been shown
that the fast drive to breathe at the beginning of exercise is
proportional to the frequency of limb movement. In attempting to
separate the contributions to the control of ventilation from central
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command and afferent feedback from locomotor muscles, ventilation
was measured in a group of subjects as they ran at two different
speeds on a treadmill.1 When the subjects started running at a given
constant speed, their ventilation immediately increased in proportion
to the treadmill speed. However, when subjects began running at a
lower speed, but with the grade elevated to match the workload of the
faster flat (0 grade) condition, their ventilation first increased to match
the slower speed and then gradually drifted up to meet their actual
oxygen demand. The immediate increase in ventilation was partially
controlled by afferent feedback from the limbs, but the subsequent
gradual increase in ventilation suggested that increased ventilation is
a response to metabolic changes and increased metabolic demand
from the exercising muscle.
RESEARCH PERSPECTIVE 7.4
Regular Exercise Reduces
Mortality
Respiratory
Disease
Pneumonia, an infection that causes inflammation of the air sacs in the lungs,
is the leading cause of infection-related death in the United States. The risk of
pneumonia increases with age and comorbid conditions such as heart
disease, chronic lung disease, and use of immunosuppressive drugs. Multiple
health benefits have been attributed to regular physical activity; however, it
remains unclear whether these benefits extend to decreased risk of respiratory
disease. Certainly, reductions in the risk of pneumonia would be consistent
with concept that regular exercise prevents age-related declines in function.
A 2014 report examined the association of running and walking with
mortality due to respiratory disease in the National Walkers’ and Runners’
Health Studies, a prospective epidemiological cohort of over 150,000 adults.6
This large cohort was used to test the hypothesis that greater exercise energy
expenditure would be associated with a lower risk for respiratory diseases in
general and pneumonia in particular. The results provided strong support for a
reduction in the risk for respiratory diseases and pneumonia as underlying and
contributing causes of mortality with greater exercise energy expenditure. Not
surprisingly, this relation was dose dependent, with more substantial
reductions in risk occurring in those with greater levels of habitual activity.
Interestingly, this risk reduction was not different between walkers and
runners. In addition, these effects appear to be independent of the effects of
exercise on cardiovascular disease risk. These findings add to the compelling
evidence for the health benefits of regular aerobic exercise.
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More recently, scientists have been interested in whether afferent
neural feedback from the limbs continues throughout exercise.
Investigators at the University of Toronto had subjects independently
alter either their pedal cadence or resistance while cycling during two
different trials.2 During one, they varied their pedal speed in a
sinusoidal manner while keeping their total workload constant, and
during the other one, they kept their speed constant while varying
their pedal workload sinusoidally (see figure 7.15). During the trial in
which pedal speed varied (figure 7.15a), there was a much faster
increase in ventilation that preceded any changes in heart rate. In
contrast, when subjects altered their workload (figure 7.15b) but kept
their pedal speed constant, there was a greater lag time before the
increase in ventilation, such that the metabolic changes preceded
changes in ventilation. The results from these unique experiments
suggest that limb movement frequency influences ventilation at the
start of, and throughout, exercise. Continued afferent neural feedback
from the limbs influences the drive to breathe during exercise.
441
FIGURE 7.15 Sine wave exercise experiments. (a) Breath-by-breath variables measured during an
exercise test with the subject varying pedaling speed (cadence) while pedal loading remains constant.
The solid lines are fitted sine waves. (b) Breath-by-breath variables measured during an exercise test
with varying pedal loading while pedaling speed (cadence) remains constant.
Reprinted by permission of J. Duffin, “The Fast Exercise Drive to Breathe,” Journal of Physiology 592 (2014): 445451.
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IN CLOSING
In chapter 6, we discussed the role of the cardiovascular system during
exercise. In this chapter, we looked at the role played by the respiratory system.
The entire process of respiration involves pulmonary ventilation (inspiration and
expiration), diffusion of gases at the alveoli, transport of gases through the
blood, and gas exchange at the tissues. In the next chapter, we examine how
the cardiovascular and respiratory systems respond to an acute bout of
exercise.
KEY TERMS
alveoli
arterial–mixed venous oxygen difference, or (a- )O2 difference
arterial–venous oxygen difference, or (a-v)O2 difference
Boyle’s gas law
Dalton’s law
dead space
expiration
external respiration
Fick’s law
Henry’s law
inspiration
internal respiration
myoglobin
oxygen cascade
oxygen diffusion capacity
partial pressure
pulmonary diffusion
pulmonary ventilation
residual volume (RV)
respiratory centers
respiratory membrane
respiratory pump
spirometry
tidal volume
total lung capacity (TLC)
vital capacity (VC)
STUDY QUESTIONS
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1.
2.
3.
Describe and differentiate between external and internal respiration.
4.
Explain the concept of partial pressures of respiratory gases—oxygen,
carbon dioxide, and nitrogen. What is the role of gas partial pressures in
pulmonary diffusion?
5.
Where in the lung does the exchange of gases with the blood occur?
Describe the role of the respiratory membrane.
6.
7.
How are oxygen and carbon dioxide transported in the blood?
8.
How is oxygen unloaded from the arterial blood to the muscle and carbon
dioxide removed from the muscle into the venous blood?
9.
What is meant by the arterial–mixed venous oxygen difference? How and
why does this change from resting conditions to exercise conditions?
10.
Describe how pulmonary ventilation is regulated. What are the chemical
stimuli that control the depth and rate of breathing? How do they control
respiration during exercise?
Describe the mechanisms involved in inspiration and expiration.
What is a spirometer? Describe and define the lung volumes measured
using spirometry.
Describe the oxygen cascade from dry ambient air to the tissues and into
the venous circulation. Provide appropriate values for the various partial
pressures of oxygen at each level.
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
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445
8
Cardiorespiratory Responses to Acute
Exercise
In this chapter and in the web study guide
Cardiovascular Responses to Acute Exercise
Heart Rate
Stroke Volume
Cardiac Output
The Fick Equation
The Cardiac Response to Exercise
Blood Pressure
Blood Flow
Blood
The Integrated Cardiovascular Response to Exercise
AUDIO FOR FIGURE 8.2 describes the use of a submaximal exercise test to estimate maximal exercise
capacity.
VIDEO 8.1 presents Ben Levine on physiological differences in trained versus untrained people and the
relationship between cardiac output and oxygen use.
AUDIO FOR FIGURE 8.9 describes an example of cardiovascular drift.
ANIMATION FOR FIGURE 8.12 details the integrated cardiovascular response to exercise.
ACTIVITY 8.1 Cardiovascular Response to Exercise reviews cardiovascular changes occurring during
exercise.
ACTIVITY 8.2 Cardiovascular Response Scenarios explores how cardiovascular responses contribute
to real-life situations.
Respiratory Responses to Acute Exercise
Pulmonary Ventilation During Dynamic Exercise
Breathing Irregularities During Exercise
Ventilation and Energy Metabolism
Respiratory Limitations to Performance
Respiratory Regulation of Acid–Base Balance
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ACTIVITY 8.3 Pulmonary Ventilation During Exercise investigates the response of pulmonary ventilation
to exercise and the factors that affect the phases of pulmonary ventilation.
ACTIVITY 8.4 Pulmonary Ventilation and Energy Metabolism reviews the key terms related to
pulmonary ventilation and energy metabolism.
In Closing
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C
ompleting a full 26.2 mi (42 km) marathon is a major accomplishment, even
for those who are young and extremely fit. On May 5, 2002, Greg Osterman
completed the Cincinnati Flying Pig Marathon, his sixth full marathon, finishing in a
time of 5 h and 16 min. This is certainly not a world record time, or even an
exceptional time for fit runners. However, in 1990 at the age of 35, Greg had
contracted a viral infection that went right to his heart and progressed to heart
failure. In 1992, he received a heart transplant. In 1993, his body started rejecting
his new heart and he also contracted leukemia, not an uncommon response to the
antirejection drugs given to transplant patients. He miraculously recovered and
started his quest to get physically fit. He ran his first race (15K) in 1994, followed by
five marathons in Bermuda, San Diego, New York, and Cincinnati in 1999 and 2001.
Greg is an excellent example of both human resolve and physiological adaptability.
After reviewing the basic anatomy and physiology of the
cardiovascular and respiratory systems, this chapter looks specifically
at how these systems respond to the increased demands placed on
the body during acute exercise. With exercise, oxygen demand by the
active muscles increases significantly. Metabolic processes speed up
and more waste products are created. During prolonged exercise or
exercise in a hot environment, body temperature increases. In
intense exercise, H+ concentration increases in the muscles and
blood, lowering their pH.
Cardiovascular Responses to Acute Exercise
Numerous interrelated cardiovascular changes occur during dynamic
exercise. The primary goal of these adjustments is to increase blood
flow to working muscle; however, cardiovascular control of virtually
every tissue and organ in the body is also altered. To better
understand the changes that occur, we must examine the function of
both the heart and the peripheral circulation. In this section, we
examine changes in all components of the cardiovascular system
from rest to acute exercise, looking specifically at the following:
Heart rate
Stroke volume
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Cardiac output
Blood pressure
Blood flow
The blood
We then see how these changes are integrated to maintain adequate
blood pressure and provide for the exercising body’s needs.
Heart Rate
Heart rate (HR) is one of the simplest physiological responses to
measure and yet one of the most informative in terms of
cardiovascular stress and strain. Measuring HR involves simply
taking the subject’s pulse, usually at the radial or carotid artery. Heart
rate is a good indicator of relative exercise intensity.
Resting Heart Rate
Resting heart rate (RHR) averages 60 to 80 beats/min in most
individuals. In highly conditioned, endurance-trained athletes, resting
rates as low as 28 beats/min have been reported. This is mainly due
to an increase in parasympathetic (vagal) tone that accompanies
endurance exercise training. Resting heart rate can also be affected
by environmental factors; for example, it increases with extremes in
temperature and altitude.
Just before the start of exercise, preexercise HR usually increases
above normal resting values. This is called the anticipatory response.
This response is mediated through release of the neurotransmitter
norepinephrine from the sympathetic nervous system and the
hormone epinephrine from the adrenal medulla. Vagal tone also
decreases. Because preexercise HR is elevated, reliable estimates of
the true RHR should be made only under conditions of total
relaxation, such as early in the morning before the subject rises from
a restful night’s sleep.
Heart Rate During Exercise
When exercise begins, HR increases directly in proportion to the
increase in exercise intensity (figure 8.1), until near-maximal exercise
is achieved. As maximal exercise intensity is approached, HR begins
to plateau even as the exercise workload continues to increase. This
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indicates that HR is approaching a maximal value. The maximum
heart rate (HRmax) is the highest HR value achieved in an all-out
effort to the point of volitional fatigue. Once accurately determined,
HRmax is a highly reliable value that remains constant from day to day.
However, this value changes slightly from year to year due to a
normal age-related decline.
HRmax is often estimated based on age because HRmax shows a
slight but predictable decrease of about one beat per year beginning
at 10 to 15 years of age. Subtracting one’s age from 220 beats/min
provides a reasonable approximation of one’s predicted HRmax.
However, this is only an estimate—individual values vary
considerably from this average value. To illustrate, for a 40-year-old
woman, HRmax would be estimated to be 180 beats/min (HRmax = 220
− 40 beats/min). However, 68% of all 40-year-olds have actual HRmax
values between 168 and 192 beats/min (mean ± 1 standard
deviation), and 95% fall between 156 and 204 beats/min (mean ± 2
standard deviations). This demonstrates the potential for error in
estimating a person’s HRmax. A similar but more accurate equation
has been developed to estimate HRmax from age. In this equation,
HRmax = 208 − (0.7 × age).16
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FIGURE 8.1 Changes in heart rate (HR) as a subject progressively walks, jogs, and then runs on a
treadmill as intensity is increased. Heart rate is plotted against exercise intensity shown as a percentage
of the subject’s O2max, at which point the rise in HR begins to plateau. The HR at this plateau is the
subject’s maximal HR or HRmax.
When the exercise intensity is held constant at any submaximal
workload, HR increases fairly rapidly until it reaches a plateau. This
plateau is the steady-state heart rate, and it is the optimal HR for
meeting the circulatory demands at that specific rate of work. For
each subsequent increase in intensity, HR will reach a new steadystate value within 3 min. However, the more intense the exercise, the
longer it takes to achieve this steady-state value.
The concept of steady-state heart rate forms the basis for simple
exercise tests that have been developed to estimate cardiorespiratory
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(aerobic) fitness. In one such test, individuals are placed on an
exercise device, such as a cycle ergometer, and then perform
exercise at two or three standardized exercise intensities. Those with
better cardiorespiratory endurance capacity will have a lower steadystate HR at each exercise intensity than those who are less fit. Thus,
a lower steady-state HR at a fixed exercise intensity is a valid
predictor of better cardiorespiratory fitness.
Figure 8.2 illustrates results from a submaximal graded exercise
test performed on a cycle ergometer by two different individuals of the
same age. Steady-state HR is measured at three or four distinct
workloads, and a line of best fit is drawn through the data points.
Because there is a consistent relation between exercise intensity and
energy demand, steady-state HR can be plotted against the
corresponding energy ( O2) required to do work on the cycle
ergometer. The resultant line can be extrapolated to the agepredicted HRmax to estimate an individual’s maximal exercise capacity.
In this figure, subject A has a higher fitness level than subject B
because (1) at any given submaximal intensity, this subject’s HR is
lower and (2) extrapolation to age-predicted HRmax yields a higher
estimated maximal exercise capacity ( O2max).
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FIGURE 8.2 The increase in heart rate with increasing power output on a cycle ergometer and oxygen
uptake is linear within a wide range. The predicted maximal oxygen uptake can be extrapolated using
the subject’s estimated maximum heart rate as demonstrated here for two subjects with similar
estimated maximum heart rates but quite different maximal workloads and
O2max values.
Reprinted by permission from P.O. Åstrand et al., Textbook of Work Physiology: Physiological Bases of Exercise,
4th ed. (Champaign, IL: Human Kinetics, 2003), 285.
Heart Rate Variability
Heart rate variability is a measure of the rhythmic fluctuation in HR
that occurs because of continuous changes in the sympathetic–
parasympathetic balance that controls sinus rhythm. Analysis of HR
variability has been used as a method of noninvasively evaluating the
relative contributions of the sympathetic and parasympathetic
nervous systems at rest and during exercise. During acute aerobic
exercise, many different factors contribute to increasing HR variability,
including increases in body core temperature, sympathetic nerve
activity, and respiratory rate. After a bout of acute exercise, HR
variability gradually increases compared to preexercising values due
to greater vagal tone. Moreover, changes in HR variability can be
used to assess the impact of exercise training (discussed in chapter
11), the occurrence of overtraining15 (discussed in chapter 14), and
even as a diagnostic tool in certain clinical populations12 (discussed in
chapter 20).
RESEARCH PERSPECTIVE 8.1
HUNTing for a Better Prediction of Maximal Heart Rate
Maximal heart rate (HRmax) is commonly used in clinical exercise testing and to
prescribe exercise intensity in physical training and rehabilitation settings.
HRmax can be determined with an individual exercise test to exhaustion and is
verified by a plateau of heart rate despite an increase in exercise intensity.
However, an exercise test to maximal exertion may not always be feasible,
especially in clinical settings where maximal exercise may not be safe or in
field tests where advanced equipment (such as a treadmill or stationary
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bicycle with adjustable grade or resistance) may not be available. Because of
these limitations, there is a need for accurate equations to predict HRmax.
HRmax declines linearly with age and is estimated using the common
formulas in the text of this chapter. However, scientists have suggested that
adding other factors, including sex, body mass index (BMI), smoking, and
physical activity, to prediction equations may increase their accuracy. In 2013,
a group of researchers in Norway set out to develop a new, more accurate
prediction formula for HRmax.8 To do this, the research team studied a
subpopulation of participants who were enrolled in the HUNT Fitness Study, a
large cohort designed to measure O2max in healthy Norwegian adults. To
create a new formula for HRmax, the researchers analyzed HRmax measured
during a peak O2 test, then investigated the relations between HRmax and
age, sex, physical activity status, BMI, and objectively measured aerobic
fitness.
HRmax was linearly related to age and was best predicted by the formula
HRmax = 211 − 0.64
× age
whereas the traditionally used prediction equation of
HRmax = 220 − age
(1) overestimated HRmax in young individuals, (2) best predicted actual HRmax
around age 40, and (3) increasingly underestimated HRmax as people aged.
Unexpectedly, the study team found that HRmax was adequately predicted by
age alone—accounting for body mass index, sex, smoking status, physical
activity, or
O2max did not improve the equation’s accuracy. This study
concluded that the new prediction equation HRmax = 211 − 0.64 × age most
accurately described HRmax as a function of age. However, like all prediction
formulas, the standard error of ±11 beats/min must still be taken into
consideration. Furthermore, although sex, body mass index, smoking, physical
activity, and fitness did not influence the age-related decline in HRmax across
the sample of subjects they surveyed, these factors may still influence HRmax
on an individual basis.
This new equation may be better than the quick-and-easy standard 220 −
age, but direct measurement of HRmax using a maximal exercise test is always
preferable when possible.
Heart rate, like other signals that repeat periodically over time, can
be represented by a power spectrum, which describes how much of
the signal occurs at each different frequency. HR signals are
analyzed with respect to frequency, rather than time, using a
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mathematical technique called spectral analysis. In spectral analysis,
the variability around the mean HR is separated into the contributing
frequency domains. There are many physiological influences on HR
variability frequency domains.5 Mathematically separating these
different elements of HR variability allows researchers to examine the
impact of exercise training or disease on each one of the individual
contributors. For example, with aerobic exercise training, there is an
increase in the parasympathetic control of HR, characterized by
greater vagal tone and reduced resting sympathetic nerve activity,
that affects the high-frequency domain of HR variability.
Stroke Volume
Stroke volume (SV) also changes during acute exercise to allow the
heart to meet the demands of exercise. At near-maximal and maximal
exercise intensities, as HR approaches its maximum, SV is a major
determinant of cardiorespiratory endurance capacity.
Stroke volume is determined by four factors:
1. The volume of venous blood returned to the heart (the heart
can only pump what returns)
2. Ventricular distensibility (the capacity to enlarge the ventricle,
to allow maximal filling)
3. Ventricular contractility (the inherent capacity of the ventricle to
contract forcefully)
4. Aortic or pulmonary artery pressure (the pressure against
which the ventricles must contract)
The first two factors influence the filling capacity of the ventricle,
determining how much blood fills the ventricle and the ease with
which the ventricle is filled at the available pressure. Together, these
factors determine the end-diastolic volume (EDV), sometimes
referred to as the preload. The last two characteristics influence the
ventricle’s ability to empty during systole, determining the force with
which blood is ejected and the pressure against which it must be
expelled into the arteries. The latter factor, the aortic mean pressure,
which represents resistance to blood being ejected from the left
ventricle (and to a less important extent, the pulmonary artery
pressure resistance to flow from the right ventricle), is referred to as
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the afterload. These four factors combine to determine the SV during
acute exercise.
Stroke Volume During Exercise
Stroke volume increases above resting values during exercise. Most
researchers agree that SV increases with increasing exercise
intensity up to intensities somewhere between 40% and 60% of
O2max. At that point, SV typically plateaus, remaining essentially
unchanged up to and including the point of exhaustion, as shown in
figure 8.3. However, other researchers have reported that SV
continues to increase beyond 40% to 60% O2max, even up through
maximal exercise intensities, as discussed shortly.
FIGURE 8.3 Changes in stroke volume (SV) as a subject exercises on a treadmill at increasing
intensities. Stroke volume is plotted as a function of percent
intensity up to approximately 40% to 60% of
O2max. The SV increases with increasing
O2max, before reaching a maximum (SVmax).
When the body is in an upright position, SV can approximately
double from resting to maximal values. For example, in active but
untrained individuals, SV increases from about 60 to 70 ml/beat at
rest to 110 to 130 ml/beat during maximal exercise. In highly trained
endurance athletes, SV can increase from 80 to 110 ml/beat at rest to
160 to 200 ml/beat during maximal exercise. During supine exercise,
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such as recumbent cycling, SV also increases but usually by only
about 20% to 40%—not nearly as much as in an upright position.
Why does body position make such a difference?
When the body is in the supine position, blood does not pool in the
lower extremities. Blood returns more easily to the heart in a supine
posture, which means that resting SV values are higher in the supine
position than in the upright position. Thus, the increase in SV with
maximal exercise is not as great in the supine position as in the
upright position because SV starts out higher. Interestingly, the
highest SV attainable in upright exercise is only slightly greater than
the resting value in the reclining position. The majority of the SV
increase during low to moderate intensities of exercise in the upright
position appears to be compensating for the force of gravity that
causes blood to pool in the extremities.
Although researchers agree that SV increases as exercise
intensity increases up to approximately 40% to 60% O2max, reports
about what happens after that point differ. A few studies have shown
that SV continues to increase beyond that intensity. Part of this
apparent disagreement might result from differences among studies
in the mode of exercise testing. Studies that show plateaus in the
40% to 60% O2max range typically have used cycle ergometers as
the mode of exercise. This makes intuitive sense since blood is
pooled in the legs during cycle ergometer exercise, resulting in
decreased venous return of blood from the legs. Thus, the plateau in
SV might be unique to cycling exercise.
Alternatively, in those studies in which SV continued to increase up
to maximal exercise intensities, subjects were generally highly trained
athletes. Many highly trained athletes, including highly trained cyclists
tested on a cycle ergometer, can continue to increase their SV
beyond 40% to 60% O2max, perhaps because of adaptations caused
by aerobic training. One such adaptation is an increased venous
return, which leads to better ventricular filling, and an increased force
of contraction (Frank-Starling mechanism). The increases in cardiac
output and SV with increasing work as represented by increasing HR,
in elite athletes, trained university distance runners, and untrained
university students, are illustrated in figure 8.4.
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FIGURE 8.4 Cardiac output and stroke volume responses to increasing exercise intensities measured
in untrained subjects, trained distance runners, and elite runners.
Adapted by permission from B. Zhou et al., “Stroke Volume Does Not Plateau During Graded Exercise in Elite Male
Distance Runners,” Medicine and Science in Sports and Exercise 33 (2001): 1849-1854.
Importance of Stroke Volume to
O2max
O2max is widely regarded as the single best measure of
cardiorespiratory endurance, as discussed in chapter 5. At a maximal
exercise intensity, O2max defines the upper limit of cardiovascular
function, that is,
O2max = HRmax × SVmax × (a-v)O2max.
Table 8.1 shows the stark difference in O2maxbetween an elite
athlete, a normal age-matched subject, and a cardiac patient with
mitral stenosis (a narrowing of the mitral valve). Because differences
in HRmax and (a-v)O2max among these three groups are small, it is the
ability to increase SV during maximal exercise that primarily
determines O2max.
How Does Stroke Volume Increase During Exercise?
Stroke volume increases during exercise despite the fact that there is
less time for ventricular filling, especially at high heart rates. For
example, at a resting HR of 70 beats/min, filling time between beats
is 0.55 sec. At a HR of 195 beats/min, this interval decreases to 0.12
sec.13 How does SV increase in light of less time to fill?
One explanation for the increase in SV with exercise is that the
primary factor determining SV is increased preload, or the extent to
which the ventricle stretches as it fills with blood, that is, the EDV.
When the ventricle stretches more during filling, it subsequently
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contracts more forcefully. For example, when a larger volume of blood
enters and fills the ventricle during diastole, the ventricular walls
stretch to a greater extent. To eject that greater volume of blood, the
ventricle responds by contracting more forcefully. This is referred to
as the Frank-Starling mechanism. At the level of the muscle fiber,
the greater the stretch of the myocardial cells, the more actin–myosin
cross-bridges are formed, and greater force is developed.
Additionally, SV will increase during exercise if the ventricle’s
contractility (an inherent property of the ventricle) is enhanced.
Contractility can increase by increasing sympathetic nerve stimulation
or circulating catecholamines (epinephrine, norepinephrine), or both.
An improved force of contraction can increase SV with or without an
increased EDV by increasing the ejection fraction. Finally, when mean
arterial blood pressure is low, SV is greater since there is less
resistance to outflow into the aorta. These mechanisms all combine
to determine the SV at any given intensity of dynamic exercise.
Stroke volume is much more difficult to measure than HR. Some
clinically used cardiovascular diagnostic techniques have made it
possible to determine exactly how SV changes with exercise.
Echocardiography (using sound waves) and radionuclide techniques
(tagging red blood cells with radioactive tracers) have elucidated how
the heart chambers respond to increasing oxygen demands during
exercise. With either technique, continuous images of the heart can
be taken at rest and up to near-maximal intensities of exercise.
Figure 8.5 illustrates the results of one study of normally active but
untrained subjects.9 In this study, participants were tested during both
supine and upright cycle ergometry at rest and at three exercise
intensities, which are depicted on the x-axis of figure 8.5.
When one goes from resting conditions to exercise of increasing
intensity, there is an increase in left ventricular EDV (a greater filling
or preload), which serves to increase SV through the Frank-Starling
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mechanism. There is also a decrease in the left ventricular ESV
(greater emptying), indicating an increased force of contraction.
Figure 8.5 shows that both the Frank-Starling mechanism and
increased contractility are important in increasing SV during exercise.
The Frank-Starling mechanism appears to have its greatest influence
at lower exercise intensities, and improved contractile force becomes
more important at higher exercise intensities.
Recall that HR also increases with exercise intensity. The plateau
or small decrease in left ventricular EDV at high exercise intensities
could be caused by a reduced ventricular filling time due to the high
HR. One study showed that ventricular filling time decreased from
about 500 to 700 ms at rest to about 150 ms at HRs between 150
and 200 beats/min.17 Therefore, with increasing intensities
approaching O2max (and HRmax), the diastolic filling time could be
shortened enough to limit filling. As a result, EDV might plateau or
even start to decrease.
For the Frank-Starling mechanism to increase SV, left ventricular
EDV must increase, necessitating an increased venous return to the
heart. As discussed in chapter 6, the muscle pump and respiratory
pump both aid in increasing venous return. In addition, redistribution
of blood flow and volume from inactive tissues such as the splanchnic
and renal circulations increases the available central blood volume.
FIGURE 8.5 Changes in left ventricular end-diastolic volume (EDV), end-systolic volume (ESV), and
stroke volume (SV) at rest and during low-, intermediate-, and peak-intensity exercise when the subject
is in the (a) supine and (b) upright positions. Note that SV = EDV − ESV.
Adapted from Poliner et al. (1980).
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To review, two factors that can contribute to an increase in SV with
increasing intensity of exercise are increased venous return (preload)
and increased ventricular contractility. The third factor that contributes
to the increase in SV during exercise—a decrease in afterload—
results from a decrease in total peripheral resistance. Total
peripheral resistance (TPR) decreases because of vasodilation of
the blood vessels in exercising skeletal muscle. This decrease in
afterload allows the left ventricle to expel blood against less
resistance, facilitating greater emptying of the ventricle.
Cardiac Output
Since cardiac output is the product of heart rate and stroke volume (
= HR × SV), cardiac output predictably increases with increasing
exercise intensity (figure 8.6). Resting cardiac output is approximately
5.0 L/min but varies in proportion to the size of the person. Maximal
cardiac output varies between less than 20 L/min in sedentary
individuals to 40 or more L/min in elite endurance athletes. Maximal
is a function of both body size and endurance training. The linear
relationship between cardiac output and exercise intensity is
expected because the major purpose of the increase in cardiac
output is to meet the muscles’ increased demand for oxygen. Like
O2max, when cardiac output approaches maximal exercise intensity, it
may reach a plateau (figure 8.6). In fact, it is likely that O2max is
ultimately limited by the inability of cardiac output to increase further.
VIDEO 8.1 Presents Ben Levine on physiological differences in
trained versus untrained people and the relationship between
cardiac output and oxygen use.
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The Fick Equation
In the 1870s, a cardiovascular physiologist by the name of Adolph
Fick developed a principle critical to our understanding of the basic
relationship between metabolism and cardiovascular function. In its
simplest form, the Fick principle states that the oxygen consumption
of a tissue is dependent on blood flow to that tissue and the amount
of oxygen extracted from the blood by the tissue. This principle can
be applied to the whole body or to regional circulations. Oxygen
consumption is the product of blood flow and the difference in
concentration of oxygen in the blood between the arterial blood
supplying the tissue and the venous blood draining out of the tissue—
the (a- )O2 difference. Whole-body oxygen consumption ( O2) is
calculated as the product of the cardiac output ( ) and (a- )O2
difference.
FIGURE 8.6 The cardiac output ( ) response to walking-running on a treadmill at increasing
intensities plotted as a function of percent
O2max. Cardiac output increases in direct proportion to
increasing intensity, eventually reaching a maximum (
max).
Fick equation:
O2 =
× (a- )O2 difference,
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which can be rewritten as
O2 = HR × SV × (a- )O2 difference.
This basic relationship is an important concept in exercise
physiology and comes up frequently throughout the remainder of this
book.
The Cardiac Response to Exercise
To see how HR, SV, and
vary under various conditions of rest and
exercise, consider the following example. An individual first moves
from a reclining position to a seated posture and then to standing.
Next the person begins walking, then jogging, and finally breaks into
a fast-paced run. How does the heart respond?
In a reclining position, HR is ~50 beats/min; it increases to about
55 beats/min during sitting and to about 60 beats/min during
standing. When the body shifts from a reclining to a sitting position
and then to a standing position, gravity causes blood to pool in the
legs, which reduces the volume of blood returning to the heart and
thus decreases SV. To compensate for the reduction in SV, HR
increases in order to maintain cardiac output; that is,
= HR × SV.
During the transition from rest to walking, HR increases from about
60 to about 90 beats/min. Heart rate increases to 140 beats/min with
moderate-paced jogging and can reach 180 beats/min or more with a
fast-paced run. The initial increase in HR—up to about 100 beats/min
—is mediated by a withdrawal of parasympathetic (vagal) tone.
Further increases in HR are mediated by increased activation of the
sympathetic nervous system. Stroke volume also increases with
exercise, further increasing cardiac output. These relationships are
illustrated in figure 8.7.
During the initial stages of exercise in untrained individuals,
increased cardiac output is caused by an increase in both HR and
SV. When the level of exercise exceeds 40% to 60% of the
individual’s maximal exercise capacity, SV either plateaus or
continues to increase at a much slower rate. Thus, further increases
in cardiac output are largely the result of increases in HR. Further SV
increases contribute more to the rise in cardiac output at high
intensities of exercise in highly trained athletes.
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FIGURE 8.7 Changes in (a) heart rate, (b) stroke volume, and (c) cardiac output with changes in
posture (lying supine, sitting, and standing upright) and with exercise (walking at 5 km/h [3.1 mph],
jogging at 11 km/h [6.8 mph], and running at 16 km/h [9.9 mph]).
Blood Pressure
During endurance exercise, systolic blood pressure increases in
direct proportion to the increase in exercise intensity. However,
diastolic pressure does not change significantly and may even
decrease. As a result of the increased systolic pressure, mean
arterial blood pressure increases. A systolic pressure that starts out
at 120 mmHg in a normal healthy person at rest can exceed 200
mmHg at maximal exercise. Systolic pressures of 240 to 250 mmHg
have been reported in normal, healthy, highly trained athletes at
maximal intensities of aerobic exercise.
Increased systolic blood pressure results from the increased
cardiac output that accompanies increasing rates of work. This
increase in pressure helps facilitate the increase in blood flow through
the vasculature. Also, blood pressure (that is, hydrostatic pressure) in
large part determines how much plasma leaves the capillaries,
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entering the tissues and carrying needed supplies. Thus increased
systolic pressure aids substrate delivery to working muscles.
After increasing initially, mean arterial pressure reaches a steady
state during submaximal steady-state endurance exercise. As work
intensity increases, so does systolic blood pressure. If steady-state
exercise is prolonged, the systolic pressure might start to decrease
gradually, but diastolic pressure remains constant. The slight
decrease in systolic blood pressure, if it occurs, is a normal response
and simply reflects increased vasodilation in the active muscles,
which decreases the total peripheral resistance (since mean arterial
pressure = cardiac output × total peripheral resistance).
Diastolic blood pressure changes little during submaximal dynamic
exercise; however, at maximal exercise intensities, diastolic blood
pressure may increase slightly. Remember that diastolic pressure
reflects the pressure in the arteries when the heart is at rest
(diastole). With dynamic exercise there is an overall increase in
sympathetic tone to the vasculature, causing overall vasoconstriction.
However, this vasoconstriction is blunted in the exercising muscles by
the release of local vasodilators, a phenomenon called functional
sympatholysis (discussed in chapter 6). Thus, because there is a
balance between vasoconstriction to inactive regional circulations and
vasodilation in active skeletal muscle, diastolic pressure does not
change substantially. However, in some cases of cardiovascular
disease, increases in diastolic pressure of 15 mmHg or more occur in
response to exercise and are one of several indications for
immediately stopping a diagnostic exercise test.
Upper body exercise causes a greater blood pressure response
than leg exercise at the same absolute rate of energy expenditure.
This is most likely attributable to the smaller exercising muscle mass
of the upper body compared with the lower body, plus an increased
energy demand to stabilize the upper body during arm exercise. This
difference in the systolic blood pressure response to upper and lower
body exercise has important implications for the heart. Myocardial
oxygen uptake and myocardial blood flow are directly related to the
product of HR and systolic blood pressure (SBP). This value is
referred to as the rate–pressure product (RPP), or double product
(RPP = HR × SBP). With static or dynamic resistance exercise or
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upper body dynamic exercise, the RPP is elevated, indicating
increased myocardial oxygen demand. The use of RPP as an indirect
index of myocardial oxygen demand is important in clinical exercise
testing.
Periodic blood pressure increases during resistance exercise, such
as weightlifting, can be extreme. With high-intensity resistance
training, blood pressure can briefly reach 480/350 mmHg. Very high
pressures like these are more commonly seen when the exerciser
performs a Valsalva maneuver to aid heavy lifts. This maneuver
occurs when a person tries to exhale while the mouth, nose, and
glottis are closed. This action causes an enormous increase in
intrathoracic pressure. Much of the subsequent blood pressure
increase results from the body’s effort to overcome the high internal
pressures created during the Valsalva maneuver.
In Review
Preexercise HR is not a reliable estimate of RHR because of the anticipatory HR
response.
As exercise intensity increases, HR increases proportionately, approaching HRmax
near the maximal exercise intensity.
To estimate HRmax:
HRmax = 220 − age in years, or
HRmax = 208 − (0.7
× age in years)
Stroke volume (the amount of blood ejected with each contraction) also increases
proportionately with increasing exercise intensity but usually achieves its maximal
value at about 40% to 60% of O2max in untrained individuals. Highly trained
individuals can continue to increase SV, sometimes up to maximal exercise
intensity.
Increases in HR and SV combine to increase cardiac output. Thus, more blood is
pumped during exercise, ensuring that an adequate supply of oxygen and
metabolic substrates reaches the exercising muscles and that the waste products
of muscle metabolism are cleared away.
During exercise, cardiac output increases in proportion to exercise intensity to
match the need for increased blood flow to exercising muscles.
According to the Fick equation, whole-body oxygen consumption ( O2) is
calculated as the product of the cardiac output ( ) and (a- )O2 difference.
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The ability to increase cardiac output, predominantly driven by increases in stroke
volume, is the primary determinant of O2max.
Blood Flow
Acute increases in cardiac output and blood pressure during exercise
allow for increased total blood flow to the body. These responses
facilitate increased blood to areas where it is needed, primarily the
exercising muscles. Additionally, sympathetic control of the
cardiovascular system redistributes blood so that areas with the
greatest metabolic need receive more blood than areas with low
demands.
Redistribution of Blood During Exercise
Blood flow patterns change markedly in the transition from rest to
exercise. Through the vasoconstrictor action of the sympathetic
nervous system on local arterioles, blood flow is redirected away from
areas where elevated flow is not essential to those areas that are
active during exercise (see figure 6.11). Only 15% to 20% of the
resting cardiac output goes to muscle, but during high-intensity
exercise, the muscles may receive 80% to 85% of the cardiac output.
This shift in blood flow to the muscles is accomplished primarily by
reducing blood flow to the kidneys and the so-called splanchnic
circulation (which includes the liver, stomach, pancreas, and
intestines). Figure 8.8 illustrates a typical distribution of cardiac output
throughout the body at rest and during heavy exercise. Because
cardiac output increases greatly with increasing intensity of exercise,
the values are shown both as the relative percentage of cardiac
output and as the absolute cardiac output going to each regional
circulation at rest and at three intensities of exercise.
Although several physiological mechanisms are responsible for the
redistribution of blood flow during exercise, they work together in an
integrated fashion. To illustrate this, consider what happens to blood
flow during exercise, focusing on the primary driver of the response,
namely the increased blood flow requirement of the exercising
skeletal muscles.
As exercise begins, active skeletal muscles rapidly require
increased oxygen delivery. This need is partially met through
sympathetic stimulation of vessels in those areas to which blood flow
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is to be reduced (e.g., the splanchnic and renal circulations). The
resulting vasoconstriction in those areas allows for more of the
(increased) cardiac output to be distributed to the exercising skeletal
muscles. In the skeletal muscles, sympathetic stimulation to the
constrictor fibers in the arteriolar walls also increases; however, local
dilator substances are released from the exercising muscle and
overcome sympathetic vasoconstriction, producing an overall
vasodilation in the muscle (functional sympatholysis).
FIGURE 8.8 The distribution of cardiac output at rest and during exercise (a) as a percentage of the
total cardiac output and (b) as absolute volumes.
Data from Vander, Sherman, and Luciano (1985).
Many local dilator substances are released in exercising skeletal
muscle. As the metabolic rate of the muscle tissue increases during
exercise, metabolic waste products begin to accumulate. Increased
metabolism causes an increase in acidity (increased hydrogen ions
and lower pH), carbon dioxide, and temperature in the muscle tissue.
These are some of the local changes that trigger vasodilation of, and
increasing blood flow through, the arterioles feeding local capillaries.
Local vasodilation is also triggered by the low partial pressure of
oxygen in the tissue or a reduction in oxygen bound to hemoglobin
(increased oxygen demand), the act of muscle contraction, and
possibly other vasoactive substances (including adenosine) released
as a result of skeletal muscle contraction.
When exercise is performed in a hot environment, there is also an
increase in blood flow to the skin to help dissipate the body heat. The
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sympathetic control of skin blood flow is unique in that there are
sympathetic vasoconstrictor fibers (similar to skeletal muscle) and
sympathetic active vasodilator fibers interacting over most of the skin
surface area. During dynamic exercise, as body core temperature
rises, there is initially a reduction in sympathetic vasoconstriction,
causing a passive vasodilation. Once a specific body core
temperature threshold is reached, skin blood flow begins to
dramatically increase by activation of the sympathetic active
vasodilator system. The increase in skin blood flow during exercise
promotes heat loss, because metabolic heat from deep in the body
can be released only when blood moves close to the skin. This limits
the rate of rise in body temperature, as discussed in more detail in
chapter 12.
Cardiovascular Drift
With prolonged aerobic exercise or aerobic exercise in a hot
environment at a steady-state intensity, SV gradually decreases and
HR increases. Cardiac output is well maintained, but arterial blood
pressure also declines. These alterations, illustrated in figure 8.9,
have been referred to collectively as cardiovascular drift.
Cardiovascular drift has traditionally been associated with a
progressive increase in the fraction of cardiac output directed to the
vasodilated skin to facilitate heat loss and attenuate the increase in
body core temperature. With more blood in the skin for the purpose of
cooling the body, less blood is available to return to the heart, thus
decreasing preload. There is also a small decrease in blood volume
resulting from sweating and from a generalized shift of plasma across
the capillary membrane into the surrounding tissues. These factors
combine to decrease ventricular filling pressure, which decreases
venous return to the heart and reduces the EDV. With the reduction in
EDV, SV is reduced (SV = EDV − ESV). In order to maintain cardiac
output (
in SV.
= HR × SV), HR increases to compensate for the decrease
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FIGURE 8.9 Circulatory responses to prolonged, moderately intense exercise in the upright posture in
a thermoneutral 20 °C environment, illustrating cardiovascular drift. Values are expressed as the
percentage of change from the values measured at the 10 min point of the exercise.
Adapted by permission from L.B. Rowell, Human Circulation: Regulation During Physical Stress (New York: Oxford
University Press, 1986), 230.
A more recent hypothesis has been put forth to explain
cardiovascular drift. As HR increases, there is less filling time for the
ventricles. This exercise tachycardia may lower SV under the
conditions of prolonged exercise even without peripheral
displacement of blood volume. From the available research, it is not
possible to pinpoint a single hypothesis that fully explains
cardiovascular drift, and it is likely that the two mechanisms may
interact.
Competition for Blood Supply
When the demands of exercise are added to blood flow demands for
all other systems of the body, competition for a limited available
cardiac output can occur. This competition for available blood flow
can develop among several vascular beds, depending on the specific
conditions. For example, there may be competition for available blood
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flow between active skeletal muscle and the gastrointestinal system
following a meal. McKirnan and coworkers7 studied the effects of
feeding versus fasting on the distribution of blood flow during exercise
in miniature pigs. The pigs were divided into two groups. One group
fasted for 14 to 17 h before exercise. The other group ate their
morning ration in two feedings: Half the ration was fed 90 to 120 min
before exercise and the other half 30 to 45 min before exercise. Both
groups of pigs then ran at approximately 65% of their O2max.
Blood flow to the hindlimb muscles during exercise was 18% lower
and gastrointestinal blood flow was 23% higher in the fed group than
in the fasted group. Similar results in humans suggest that the
redistribution of gastrointestinal blood flow to the working muscles is
attenuated after a meal. As a practical application, these findings
suggest that athletes should be cautious in timing their meals before
competition to maximize blood flow to the active muscles during
exercise.
Another example of the competition for blood flow is seen in
exercise in a hot environment. In this scenario, competition for
available cardiac output can occur between the skin circulation for
thermoregulation and the exercising muscles. This is discussed in
more detail in chapter 12.
Blood
We have now examined how the heart and blood vessels respond to
exercise. The remaining component of the cardiovascular system is
the blood: the fluid that carries oxygen and nutrients to the tissues
and clears away waste products of metabolism. As metabolism
increases during exercise, several aspects of the blood itself become
increasingly critical for optimal performance.
Oxygen Content
At rest, the blood’s oxygen content varies from 20 ml of oxygen per
100 ml of arterial blood to 14 ml of oxygen per 100 ml of venous
blood returning to the right atrium. The difference between these two
values (20 ml − 14 ml = 6 ml) is referred to as the arterial–mixed
venous oxygen difference, or (a- )O2 difference. This value
represents the extent to which oxygen is extracted, or removed, from
the blood as it passes through the body.
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With increasing exercise intensity, the (a- )O2 difference increases
progressively and can almost triple from rest to maximal exercise
intensities (see figure 8.10). This increased difference really reflects a
decreasing venous oxygen content, because arterial oxygen content
changes little from rest up to maximal exertion. With exercise, more
oxygen is required by the active muscles; therefore, more oxygen is
extracted from the blood. The venous oxygen content decreases,
approaching zero in the active muscles. However, mixed venous
blood in the right atrium of the heart rarely decreases below 4 ml of
oxygen per 100 ml of blood because the blood returning from the
active tissues is mixed with blood from inactive tissues as it returns to
the heart. Oxygen extraction by the inactive tissues is far lower than
in the active muscles.
FIGURE 8.10 Changes in the oxygen content of arterial and mixed venous blood and the (a- )O2
difference (arterial–mixed venous oxygen difference) as a function of exercise intensity.
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FIGURE 8.11 Filtration of plasma from the microvasculature. Both the blood pressure (PC) inside the
blood vessel and the oncotic pressure (πT) in the tissue cause plasma to flow from the intravascular
space to the interstitial space. The pressure that the tissue (PT) exerts on the blood vessel and the
oncotic pressure of the blood (πC) inside the blood vessel cause plasma to be reabsorbed. Net filtration
of plasma can be determined by summing the outward forces (PC +
forces (PT −
πT) and subtracting the inward
πC); net capillary filtration = (PC + πT) − (PT − πC).
Plasma Volume
Upon standing, or with the onset of exercise, there is an almost
immediate loss of plasma from the blood to the interstitial fluid space.
The movement of fluid out of the capillaries is dictated by the
pressures inside the capillaries, which include the hydrostatic
pressure exerted by increased blood pressure and the oncotic
pressure, the pressure exerted by the proteins in the blood, mostly
albumin. The pressures that influence fluid movement outside the
capillaries are the pressure provided by the surrounding tissue as
well as the oncotic pressures from proteins in the interstitial fluid
(figure 8.11). Osmotic pressures, those exerted by electrolytes in
solution on both sides of the capillary wall, also play a role. As blood
pressure increases with exercise, the hydrostatic pressure within the
capillaries increases. This increase in blood pressure forces water
from the intravascular compartment to the interstitial compartment.
Also, as metabolic waste products build up in the active muscle,
intramuscular osmotic pressure increases, which draws fluid out of
the capillaries to the muscle.
Approximately a 10% to 15% reduction in plasma volume can
occur with prolonged exercise, with the largest falls occurring during
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the first few minutes. During resistance training, the plasma volume
loss is proportional to the intensity of the effort, with similar transient
losses of fluid from the vascular space of 10% to 15%.
If exercise intensity or environmental conditions cause sweating,
additional plasma volume losses may occur. Although the major
source of fluid for sweat formation is the interstitial fluid, this fluid
space will be diminished as sweating continues. This increases the
oncotic (since proteins do not move with the fluid) and osmotic (since
sweat has fewer electrolytes than interstitial fluid) pressures in the
interstitial space, causing even more plasma to move out of the
vascular compartment into the interstitial space. Intracellular fluid
volume is impossible to measure directly and accurately, but research
suggests that fluid is also lost from the intracellular compartment
during prolonged exercise and even from the red blood cells, which
may shrink in size.
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A reduction in plasma volume can impair performance. For longduration activities in which dehydration occurs and heat loss is a
problem, blood flow to active tissues may be reduced to allow
increasingly more blood to be diverted to the skin in an attempt to
lose body heat. Note that a decrease in muscle blood flow occurs
only in conditions of dehydration and only at high intensities. Severely
reduced plasma volume also increases blood viscosity, which can
impede blood flow and thus limit oxygen transport, especially if the
hematocrit exceeds 60%.
In activities that last a few minutes or less, body fluid shifts are of
little practical importance. As exercise duration increases, however,
body fluid changes and temperature regulation become important for
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performance. For the football player, the Tour de France cyclist, or the
marathon runner, these processes are crucial, not only for
competition but also for survival. Deaths have occurred from
dehydration and hyperthermia during, or as a result of, various sport
activities. These issues are discussed in detail in chapter 12.
Hemoconcentration
When plasma volume is reduced, hemoconcentration occurs. When
the fluid portion of the blood is reduced, the cellular and protein
portions represent a larger fraction of the total blood volume; that is,
they
become
more
concentrated
in
the
blood.
This
hemoconcentration increases red blood cell concentration
substantially—by up to 25%. Hematocrit can increase from 40% to
50%. However, the total number and volume of red blood cells do not
change substantially.
The net effect, even without an increase in the total number of red
blood cells, is to increase the number of red blood cells per unit of
blood; that is, the cells are more concentrated. As the red blood cell
concentration increases, so does the blood’s per-unit hemoglobin
content. This substantially increases the blood’s oxygen-carrying
capacity, which is advantageous during exercise and provides a
distinct advantage at altitude, as discussed in chapter 13.
The Integrated Cardiovascular Response to Exercise
As is evident from all of the changes in cardiovascular function that
take place during exercise, the cardiovascular system is extremely
complex but responds exquisitely to deliver oxygen to meet the
demands of exercising muscle. Figure 8.12 is a simplified flow
diagram that illustrates how the body integrates all these
cardiovascular responses to provide for its needs during exercise.
Key areas and responses are labeled and summarized to help
illustrate how these complex control mechanisms are coordinated. It
is important to note that although the body attempts to meet the blood
flow needs of the muscle, it can do so only if blood pressure is not
compromised. Maintenance of arterial blood pressure appears to be
the highest priority of the cardiovascular system, regardless of
exercise, the environment, or other competing needs.
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FIGURE 8.12 The integrated cardiovascular response to exercise.
Adapted by permission from E.F. Coyle, “Cardiovascular Function During Exercise: Neural Control Factors,” Sports
Science Exchange 4, no. 34 (1991): 1-6. Adapted with permission of Stokely-Van Camp, Inc.
477
RESEARCH PERSPECTIVE 8.2
Is Recovery a Distinct Cardiovascular State?
Exercise recovery refers to the time period immediately following a bout of
exercise. This period continues until the system has completely recovered, or
returned to a resting state, and can last anywhere from seconds to hours
depending on the mode and intensity of the exercise. Exercise recovery can
also refer to the specific physiological state that exists after exercise, which is
distinctly different from the physiology of exercise or the physiology at rest.
Some of these physiological changes during recovery may be necessary for
long-term adaptation to exercise training, yet some can lead to cardiovascular
instability during recovery. Over the last 20 years, the scientific understanding
of exercise recovery as a distinct physiological state has grown immensely,
mainly through human studies of cardiovascular variables such as blood
pressure, heart rate, and cardiac output immediately following aerobic
exercise or resistance exercise.11
In general, there is a dose-dependent effect of exercise intensity and
duration on the cardiovascular changes that follow aerobic exercise. In
general, the increase in vascular conductance (or decrease in resistance due
to vasodilation of the blood vessels in the muscle) is greater than the increase
in cardiac output following a bout of aerobic exercise. This means that
peripheral vasodilation is the driving force that lowers blood pressure after
exercise. This reduced blood pressure after exercise is called postexercise
hypotension, and can last for several hours following a bout of aerobic
exercise. The sustained postexercise vasodilation occurs largely within the
previously active skeletal muscle, with a smaller but still relevant vasodilation
in the nonactive skeletal muscle beds. Blood flow to the other tissues (e.g.,
brain, gut) reverts more quickly to resting values. Vasodilation of the nonactive
skeletal muscle probably occurs due to a resetting of the blood pressure set
point at the brain, while vasodilation of the previously active skeletal muscle is
due to the release of local vasodilatory molecules. Recently, it has been
demonstrated that the one important molecule released by the previously
active muscle is histamine. Histamine is elevated in the muscle following
exercise, and postexercise vasodilation is reduced by 80% when the actions
of histamine are inhibited. While the lasting effects of histamine improve our
understanding of what causes postexercise hypotension during recovery, the
exercise-related trigger for histamine release from the muscle remains
unknown.
The cardiovascular changes that occur during recovery following a bout of
resistance exercise are distinctly different from those following acute aerobic
exercise. Like aerobic exercise, blood pressure is reduced following resistance
exercise. However, in contrast to aerobic exercise, postexercise hypotension
following resistance exercise is due to decreases in cardiac output, not to
vasodilation in the vascular beds of the previously active muscle. It is unclear
why the mechanisms controlling blood pressure during recovery are different
478
between aerobic and resistance exercise, but these differences are likely due
to both central regulation (how the sympathetic nervous system controls blood
pressure) and local cellular changes in the muscle. Interestingly, kneeextension exercise that replicates resistance training does not generate a local
increase in histamines, while knee-extension exercise that replicates aerobic
exercise does. Because combined aerobic and resistance exercise programs
do not further reduce postexercise blood pressure compared to aerobic
exercise alone, there is probably some overlap in the central mechanisms.
Overall, there are fewer studies of the control of postexercise hypotension
following resistance exercise. Although the recent research points to a larger
role for changes in the central control of blood pressure during recovery, this is
an area that requires further study.
Exercise recovery can be viewed as both a window of opportunity for the
positive adaptations to training to be manipulated and a vulnerable period in
which individuals are at heightened risk for adverse events such as fainting.
Fully understanding this period may provide insight into when the
cardiovascular system has recovered from prior training and is physiologically
ready for additional training stress. The future may include training methods
that take advantage of the exercise recovery state to avoid negative
consequences of overtraining and to optimize training and health outcomes.
The cardiovascular and respiratory adjustments to dynamic
exercise are profound and rapid. Within 1 s of the initiation of muscle
contraction, HR dramatically increases by vagal withdrawal and
respiration increases. Increases in cardiac output and blood pressure
increase blood flow to the active skeletal muscle to meet its metabolic
demands. What causes these extremely rapid early changes in the
cardiovascular system, since they take place well before metabolic
needs of working muscle occur?
Over the years there has been considerable debate over what
causes the cardiovascular system to be turned on at the onset of
exercise. One explanation is the theory of central command, which
involves parallel coactivation of both the motor and the cardiovascular
control centers of the brain. Activation of central command rapidly
increases HR and blood pressure. In addition to central command,
the cardiovascular responses to exercise are modified by
mechanoreceptors, chemoreceptors, and baroreceptors. As
discussed in chapter 6, baroreceptors are sensitive to stretch and
send information back to the cardiovascular control centers about
blood pressure. Signals from the periphery are sent back to the
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cardiovascular control centers through the stimulation of
mechanoreceptors that are sensitive to the stretch of the skeletal
muscle and through the chemoreceptors that are sensitive to an
increase in metabolites in the muscle. Feedback about blood
pressure and the local muscle environment helps to fine-tune and
adjust the cardiovascular response. These relationships are
illustrated in figure 8.13.
FIGURE 8.13 A summary of cardiovascular (CV) control during exercise.
Adapted by permission from S.K. Powers & E.T. Howley, Exercise Physiology: Theory and Application to Fitness
and Performance, 5th ed. (New York, McGraw-Hill, 2004), 188. © The McGraw-Hill Education.
In Review
Mean arterial blood pressure increases immediately in response to exercise, and
the magnitude of the increase is proportional to the intensity of exercise. During
whole-body endurance exercise, this is accomplished primarily by an increase in
systolic blood pressure, with minimal changes in diastolic pressure.
Systolic blood pressure can exceed 200 to 250 mmHg at maximal exercise
intensity, the result of increases in cardiac output. Upper body exercise causes a
greater blood pressure response than leg exercise at the same absolute rate of
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energy expenditure, likely due to the smaller muscle mass involved and the need
to stabilize the trunk during dynamic arm exercise.
Blood flow is redistributed during exercise from inactive or low-activity tissues of
the body like the liver and kidneys to meet the increased metabolic needs of
exercising muscles.
With prolonged aerobic exercise, or aerobic exercise in the heat, SV gradually
decreases and HR increases proportionately to maintain cardiac output. This is
referred to as cardiovascular drift and is associated with a progressive increase in
blood flow to the vasodilated skin and losses of fluid from the vascular space.
The changes that occur in the blood during exercise include the following:
1.
The (a- )O2 difference increases as venous oxygen concentration
decreases, reflecting increased extraction of oxygen from the blood for use
by the active tissues.
2.
Plasma volume decreases. Plasma is pushed out of the capillaries by
increased hydrostatic pressure as blood pressure increases, and fluid is
drawn into the muscles by the increased oncotic and osmotic pressures in the
muscle tissues, a by-product of metabolism. With prolonged exercise or
exercise in hot environments, increasingly more plasma volume is lost
through sweating.
3.
Hemoconcentration occurs as plasma volume (water) decreases. Although
the actual number of red blood cells stays relatively constant, the relative
number of red blood cells per unit of blood increases, which increases
oxygen-carrying capacity.
Respiratory Responses to Acute Exercise
Now that we have discussed the role of the cardiovascular system in
delivering oxygen to the exercising muscle, we examine how the
respiratory system responds to acute dynamic exercise.
Pulmonary Ventilation During Dynamic Exercise
The onset of exercise is accompanied by an immediate increase in
ventilation. In fact, like the HR response, the marked increase in
breathing may occur even before the onset of muscular contractions
—that is, it may be an anticipatory response. This is shown in figure
8.14 for light, moderate, and heavy exercise. Because of its rapid
onset, this initial respiratory adjustment to the demands of exercise is
undoubtedly neural in nature, mediated by respiratory control centers
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in the brain (central command), although neural signals also come
from receptors in the exercising muscle.
FIGURE 8.14 The ventilatory response to light, moderate, and heavy exercise. The subject exercised
at each of the three intensities for 5 min. After an initial steep increase, the ventilation rate tended to
plateau at a steady-state value at the light and moderate intensities but continued to increase somewhat
at the heavy intensity.
The more gradual second phase of the respiratory increase shown
during heavy exercise in figure 8.14 is controlled primarily by changes
in the chemical status of the arterial blood. As exercise progresses,
increased metabolism in the muscles generates more CO2 and H+.
Recall that these changes shift the oxyhemoglobin saturation curve
rightward, enhancing oxygen unloading in the muscles, which
increases the (a- )O2 difference. Increased CO2 and H+ are sensed
by chemoreceptors primarily located in the brain, carotid bodies, and
lungs, which in turn stimulate the inspiratory center, increasing rate
and depth of respiration. Chemoreceptors in the muscles themselves
might also be involved. In addition, receptors in the right ventricle of
the heart send information to the inspiratory center so that increases
in cardiac output can stimulate breathing during the early minutes of
exercise. The influences of CO2 and H+ concentrations in the blood
on breathing rate and pattern serve to fine-tune the neutrally
mediated respiratory response to exercise in order to precisely match
oxygen delivery with aerobic demands without overtaxing respiratory
muscles.
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RESEARCH PERSPECTIVE 8.3
Posture Affects Ventilation During Recovery After
Exercise
Body posture affects cardiopulmonary function due to the effects of gravity.
For example, in the upright posture, the mechanical actions of the inspiratory
muscles expand the chest wall and elevate the rib cage against gravity, while
changing to the supine posture increases abdominal pressure on the pleural
cavity and inspiration is achieved predominantly through abdominal
expansion. Despite reports that cardiopulmonary function is affected by body
position, few exercise physiologists have investigated the effect of posture
during recovery from aerobic exercise.
A 2017 study conducted in Korea examined cardiopulmonary function in
relation to body position during recovery from a maximal exercise test.4
Subjects were randomly assigned to one of three recovery postures: supine,
sitting, or sitting with the trunk leaning forward. Each subject performed a
maximal exercise test to exhaustion, then immediately assumed their
assigned recovery position. Oxygen uptake, minute ventilatory volume,
respiration rate, and heart rate were measured during the assigned posture at
rest before the test and at 1, 3, and 5 min of recovery. No differences in these
variables were seen preexercise. While there were no differences in heart or
respiratory rate between recovery postures, the O2 and minute ventilatory
volume were significantly lower during recovery in the group assigned to the
trunk-leaning-forward posture. This forward-leaning posture improves
ventilatory capacity during recovery from maximal exercise, which, in turn,
enables rapid recovery of the respiratory system after exercise. The study
team concluded that the forward-leaning position has a positive effect on
pulmonary ventilation after exercise and may be the most effective posture to
promote recovery of breathing after maximal exertion.
Pulmonary ventilation increases during exercise in direct
proportion to the metabolic needs of exercising muscle. At low
exercise intensities, this is accomplished by increases in tidal volume
(the amount of air moved in and out of the lungs during regular
breathing). At higher intensities, the rate of respiration also increases.
Maximal rates of pulmonary ventilation depend on body size. Maximal
ventilation rates of approximately 100 L/min are common for smaller
individuals but may exceed 200 L/min in larger individuals.
At the end of exercise, the muscles’ energy demands decrease
almost immediately to resting levels. But pulmonary ventilation
returns to normal at a slower rate. If the rate of breathing perfectly
483
matched the metabolic demands of the tissues, respiration would
decrease to the resting level within seconds after exercise. But
respiratory recovery takes several minutes, which suggests that
postexercise breathing is regulated primarily by acid–base balance,
the partial pressure of dissolved carbon dioxide (PCO2), and blood
temperature.
Breathing Irregularities During Exercise
Ideally, breathing during exercise is regulated in a way that
maximizes aerobic performance. However, respiratory dysfunction
during exercise can hinder performance.
Dyspnea
The sensation of dyspnea (shortness of breath) during exercise is
common among individuals with poor aerobic fitness levels who
attempt to exercise at intensities that significantly elevate arterial CO2
and H+ concentrations. As discussed in chapter 7, both stimuli send
strong signals to the inspiratory center to increase the rate and depth
of ventilation. Although exercise-induced dyspnea is sensed as an
inability to breathe, the underlying cause is an inability to adjust
breathing to blood PCO2 and H+.
Failure to reduce these stimuli during exercise appears to be
related to poor conditioning of respiratory muscles. Despite a strong
neural drive to ventilate the lungs, the respiratory muscles fatigue
easily and are unable to reestablish normal homeostasis.
Exercise-Induced Asthma
In healthy humans, the respiratory system in general and the ability to
conduct efficient gas exchange at the lungs in particular do not
normally limit exercise performance. However, it is estimated that up
to 55% of elite athletes participating in endurance winter sports and
swimming experience symptoms of exercise-induced asthma (EIA),
exercise-induced bronchospasm (EIB), or both.1,6 Exercise-induced
asthma is defined as a lower airway obstruction with symptoms that
include coughing, wheezing, or dyspnea that is induced by exercise
in individuals with underlying asthma. In addition to EIA, EIB is a
reduction in lung function measured by the forced expiratory volume
in one second (FEV1) performed after a standardized exercise test.
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Many athletes experience these respiratory symptoms, and the onset
can occur during childhood or later in life during their sport careers.
Physiologically, there are several different mechanisms by which
EIA and EIB may occur in athletes. The classic reasoning has been
that hyperventilation during intense exercise leads to increased
evaporation of water from the airway surface. This is a result of
having to humidify and warm the air coming into the lung coupled with
an increased rate of ventilation during intense exercise. The
evaporation of water leads to an increase in osmolality, providing a
stimulus for water to move from inside cells to the extracellular fluid.
485
This shrinkage of cells then induces inflammation, in turn causing the
airways to constrict.
Other proposed contributors to EIA and EIB in athletes include a
disruption to the airway epithelium and microvasculature injury
induced by strenuous exercise and airway cooling. Airway cooling
causes a reflex increase in parasympathetic nerve activity, causing
bronchoconstriction and vasoconstriction of the blood vessels in the
bronchioles in order to conserve heat.
Some aspects of EIA and EIB in elite athletes relate to the specific
environmental and sport-specific training conditions in which
symptoms occur. For example, the cold and dry air that accompanies
winter sports,6 the ultrafine airborne particles emitted from ice
resurfacing machines in indoor ice rinks,14 the pollen and pollutant
exposure in athletes practicing outdoors,2 and chemical exposure in
chlorine-rich atmospheres for swimmers have all been implicated as
causal factors in breathing problems of athletes.
Hyperventilation
The anticipation of or anxiety about exercise, as well as some
respiratory disorders, can cause an increase in ventilation in excess
of that needed to support exercise. Such overbreathing is termed
hyperventilation. At rest, hyperventilation can decrease the normal
PCO2 of 40 mmHg in the alveoli and arterial blood to about 15 mmHg.
As arterial CO2 concentrations decrease, blood pH increases. These
effects combine to reduce the ventilatory drive. Because the blood
leaving the lungs is almost always about 98% saturated with oxygen,
an increase in the alveolar PO2 does not increase the oxygen content
of the blood. Consequently, the reduced drive to breathe—along with
the improved ability to hold one’s breath after hyperventilating—
results from carbon dioxide unloading rather than increased blood
oxygen. This is sometimes referred to as “blowing off CO2.” Even
when performed for only a few seconds, such deep, rapid breathing
can lead to light-headedness and even loss of consciousness. This
phenomenon reveals the sensitivity of the respiratory system’s
regulation by carbon dioxide and pH.
Valsalva Maneuver
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The Valsalva maneuver is a potentially dangerous respiratory
procedure that frequently accompanies certain types of exercise, in
particular the lifting of heavy objects. This occurs when the individual
closes the glottis (the opening between the vocal cords),
increases the intra-abdominal pressure by forcibly contracting
the diaphragm and the abdominal muscles, and
increases the intrathoracic pressure by forcibly contracting the
respiratory muscles.
As a result of these actions, air is trapped and pressurized in the
lungs. The high intra-abdominal and intrathoracic pressures restrict
venous return by collapsing the great veins. This maneuver, if held for
an extended period of time, can greatly reduce the volume of blood
returning to the heart, decreasing cardiac output and lowering arterial
blood pressure. Although the Valsalva maneuver can be helpful in
certain circumstances, the maneuver can be dangerous and should
be avoided.
Ventilation and Energy Metabolism
During long periods of mild steady-state activity, ventilation matches
the rate of energy metabolism, varying in proportion to the volume of
oxygen consumed and the volume of carbon dioxide produced ( O2
and CO2, respectively) by the body.
Ventilatory Equivalent for Oxygen
The ratio between the volume of air expired or ventilated ( E) and the
amount of oxygen consumed by the tissues ( O2) in a given amount
of time is referred to as the ventilatory equivalent for oxygen ( . It
is typically measured in liters of air breathed per liter of oxygen
consumed per minute.
At rest, the E/ O2 can range from 23 to 28 L of air per liter of
oxygen. This value changes very little during mild exercise, such as
walking. But when exercise intensity increases to near-maximal
levels, the E/ O2 can be greater than 30 L of air per liter of oxygen
consumed. In general, however, the
E/ O2 remains relatively
constant over a wide range of exercise intensities, indicating that the
487
control of breathing is properly matched to the body’s demand for
oxygen.
Ventilatory Threshold
As exercise intensity increases, at some point ventilation increases
disproportionately to oxygen consumption. The point at which this
occurs, typically between ~55% and 70% of O2max, is called the
ventilatory threshold, illustrated in figure 8.15. At approximately the
same intensity as the ventilatory threshold, more lactate starts to
appear in the blood. This may result from greater production of
lactate or less clearance of lactate or both. This lactic acid combines
with sodium bicarbonate (which buffers acid) and forms sodium
lactate, water, and carbon dioxide. As we know, the increase in
carbon dioxide stimulates chemoreceptors that signal the inspiratory
center to increase ventilation. Thus, the ventilatory threshold reflects
the respiratory response to increased carbon dioxide levels.
Ventilation increases dramatically beyond the ventilatory threshold, as
seen in figure 8.15.
The disproportionate increase in ventilation without an equivalent
increase in oxygen consumption led to early speculation that the
ventilatory threshold might be related to the lactate threshold (that
point at which blood lactate production exceeds lactate reuptake and
clearance as described in chapter 5). The ventilatory threshold
reflects a disproportionate increase in the volume of carbon dioxide
produced per minute ( CO2) relative to the oxygen consumed. Recall
from chapter 5 that the respiratory exchange ratio (RER) is the ratio
of carbon dioxide production to oxygen consumption. Thus, the
disproportionate increase in carbon dioxide production also causes
RER to increase.
The increased CO2 was thought to result from excess carbon
dioxide being released from bicarbonate buffering of lactic acid.
Wasserman and McIlroy18 coined the term anaerobic threshold to
refer to this phenomenon because they assumed that the sudden
increase in CO2 reflected a shift toward more anaerobic metabolism.
They believed that this was a good noninvasive alternative to blood
sampling for detecting the onset of anaerobic metabolism. It should
488
be noted that a number of scientists objected to their use of the term
anaerobic threshold to refer to this respiratory phenomenon.
FIGURE 8.15 Changes in pulmonary ventilation (
the concept of ventilatory threshold.
E)
during running at increasing velocities, illustrating
Over the years, the anaerobic threshold concept has been refined
considerably to provide a relatively accurate estimate of lactate
threshold. One of the more accurate techniques for identifying this
threshold involves monitoring both the ventilatory equivalent for
oxygen ( E/ O2) and the ventilatory equivalent for carbon dioxide
( E/ CO2), which is the ratio of the volume of air expired ( E) to the
volume of carbon dioxide produced ( CO2). Using this technique, the
threshold is defined as that point where there is a systematic increase
in E/ O2 without a concomitant increase in E/ CO2. This is
illustrated in figure 8.16. Both the E/ CO2 and E/ O2 decline with
increasing exercise intensity at the lower intensities. However, the E/
O2 starts to increase at about 75 W while the E/ CO2 continues to
decline. This indicates that the increase in ventilation to remove CO2
is disproportionate to the body’s need to provide O2. In general, this
respiratory threshold technique provides a reasonably close estimate
of the lactate threshold, eliminating the need for repeated blood
sampling.
489
FIGURE 8.16 Changes in the ventilatory equivalent for carbon dioxide (
equivalent for oxygen (
E/
E/
CO2) and the ventilatory
O2) during increasing intensities of exercise on a cycle ergometer. Note that
the breakpoint of the estimated lactate threshold at a power output of 75 W is evident only in the
E/
O2 ratio.
Respiratory Limitations to Performance
Like all tissue activity, respiration requires energy. Most of this energy
is used by the respiratory muscles during pulmonary ventilation. At
rest, the respiratory muscles account for only about 2% of the total
oxygen uptake. As the rate and depth of ventilation increase, so does
the energy cost of respiration. The diaphragm, the intercostal
muscles, and the abdominal muscles can account for up to 11% of
the total oxygen consumed during heavy exercise and can receive up
to 15% of the cardiac output. During recovery from dynamic exercise,
sustained elevations in ventilation continue to demand increased
energy, accounting for 9% to 12% of the total oxygen consumed
postexercise.
In Review
During exercise, ventilation shows an almost immediate increase due to increased
inspiratory center stimulation. This is caused by both central command and neural
feedback from muscle activity itself. This phase is followed by a plateau (during
light exercise) or a much more gradual increase in respiration (during heavy
exercise) that results from chemical changes in the arterial blood resulting from
exercise metabolism.
490
Altered breathing patterns and sensations associated with exercise include
dyspnea, exercise-induced asthma or bronchospasm, hyperventilation, and
performance of the Valsalva maneuver.
During mild, steady-state exercise, ventilation increases to match the rate of
energy metabolism; that is, ventilation parallels oxygen uptake. The ratio of air
ventilated to oxygen consumed is the ventilatory equivalent for oxygen ( E/ O2).
At low exercise intensities, increased ventilation is accomplished by increases in
tidal volume (the amount of air moved in and out of the lungs during regular
breathing). At higher intensities, the rate of respiration also increases.
Maximal rates of pulmonary ventilation depend on body size. Maximal ventilation
rates of approximately 100 L/min are common for smaller individuals but may
exceed 200 L/min in larger individuals.
The ventilatory threshold is the point at which ventilation begins to increase
disproportionately to the increase in oxygen consumption. This increase in E
reflects the need to remove excess carbon dioxide.
We can estimate lactate threshold with reasonable accuracy by identifying that
point at which E/ O2 starts to increase while E/ CO2 continues to decline.
Although the muscles of respiration are heavily taxed during
exercise, ventilation is sufficient to prevent an increase in alveolar
PCO2 or a decline in alveolar PO2 during activities lasting only a few
minutes. Even during maximal effort, ventilation usually is not pushed
to its maximal capacity to voluntarily move air in and out of the lungs.
This capacity is called the maximal voluntary ventilation and is
significantly greater than ventilation at maximal exercise. However,
considerable evidence suggests that pulmonary ventilation might be a
limiting factor during exercise of very high intensity (95%-100%
O2max) in highly trained subjects.
Can heavy breathing for several hours (such as during marathon
running) cause glycogen depletion and fatigue of the respiratory
muscles? Animal studies have shown a substantial sparing of their
respiratory muscle glycogen compared with muscle glycogen in
exercising muscles. Although similar data are not available for
humans, our respiratory muscles are better designed for long-term
activity than are the muscles in our extremities. The diaphragm, for
example, has two to three times more oxidative capacity (oxidative
enzymes and mitochondria) and capillary density than other skeletal
491
muscle. Consequently, the diaphragm can obtain more energy from
oxidative sources than can skeletal muscles.
Similarly, airway resistance and gas diffusion in the lungs do not
limit exercise in a normal, healthy individual. The volume of air
inspired can increase 20- to 40-fold with exercise—from ~5 L/min at
rest up to 100 to 200 L/min with maximal exertion. Airway resistance,
however, is maintained at near-resting levels by airway dilation
(through an increase in the laryngeal aperture and bronchodilation).
During submaximal and maximal efforts in untrained and moderately
trained individuals, blood leaving the lungs remains nearly saturated
with oxygen (~98%). However, with maximal exercise in some highly
trained elite endurance athletes, there is too large a demand on lung
gas exchange, resulting in a decline in arterial PO2 and arterial
oxygen saturation (i.e., exercise-induced arterial hypoxemia
[EIAH]). Approximately 40% to 50% of elite endurance athletes
experience a significant reduction in arterial oxygenation during
exercise approaching exhaustion.10 Arterial hypoxemia at maximal
exercise is likely the result of a mismatch between ventilation and
perfusion of the lung. Since cardiac output is extremely high in elite
athletes, blood is flowing through the lungs at a high rate and thus
there may not be sufficient time for that blood to become saturated
with oxygen. Thus, in healthy individuals, the respiratory system is
well designed to accommodate the demands of heavy breathing
during short- and long-term physical effort. However, some highly
trained individuals who consume unusually large amounts of oxygen
during exhaustive exercise can face respiratory limitations.
The respiratory system also can limit performance in patient
populations with restricted or obstructed airways. For example,
asthma causes constriction of the bronchial tubes and swelling of the
mucous membranes. These effects cause considerable resistance to
ventilation, resulting in a shortness of breath. Exercise is known to
bring about symptoms of asthma or to worsen those symptoms in
select individuals. The mechanism or mechanisms through which
exercise induces airway obstruction in individuals with so-called
exercise-induced asthma remain unknown, despite extensive study.
In Review
492
Respiratory muscles can account for up to 10% of the body’s total oxygen
consumption and 15% of the cardiac output during heavy exercise.
Pulmonary ventilation is usually not a limiting factor for performance even during
maximal effort, although it can limit performance in some elite endurance athletes.
The respiratory muscles are well designed to avoid fatigue during long-term
activity.
Airway resistance and gas diffusion usually do not limit performance in normal,
healthy individuals exercising at sea level.
The respiratory system can, and often does, limit performance in people with
various types of restrictive or obstructive respiratory disorders.
Respiratory Regulation of Acid–Base Balance
As noted earlier, high-intensity exercise results in the production and
accumulation of lactate and H+. Although regulation of acid–base
balance involves more than control of respiration, it is discussed here
because the respiratory system plays such a crucial role in rapid
adjustment of the body’s acid–base status during and immediately
after exercise.
Acids, such as lactic acid and carbonic acid, release hydrogen ions
(H+). As noted in the preceding chapters, the metabolism of
carbohydrate, fat, or protein produces inorganic acids that dissociate,
increasing the H+ concentration in body fluids, thus lowering the pH.
To minimize the effects of free H+, the blood and muscles contain
base substances that combine with, and thus buffer or neutralize, the
H+:
H+ + buffer → H-buffer
Under resting conditions, body fluids have more bases (such as
bicarbonate, phosphate, and proteins) than acids, resulting in a
slightly alkaline tissue pH that ranges from 7.1 in muscle to 7.4 in
arterial blood. The tolerable limits for arterial blood pH extend from
6.9 to 7.5, although the extremes of this range can be tolerated only
for a few minutes (see figure 8.17). An H+ concentration above
normal (low pH) is referred to as acidosis, whereas a decrease in H+
below the normal concentration (high pH) is termed alkalosis.
493
FIGURE 8.17 Tolerable limits for arterial blood pH and muscle pH at rest and at exhaustion. Note the
small range of physiological tolerance for both muscle and blood pH.
The pH of intra- and extracellular body fluids is kept within a
relatively narrow range by
chemical buffers in the blood,
pulmonary ventilation, and
kidney function.
The three major chemical buffers in the body are bicarbonate
(HCO3−), inorganic phosphates (Pi), and proteins. In addition to these,
hemoglobin in the red blood cells is also a major buffer. Table 8.2
illustrates the relative contributions of these buffers in handling acids
in the blood. Recall that bicarbonate combines with H+ to form
carbonic acid, thereby eliminating the acidifying influence of free H+.
The carbonic acid in turn forms carbon dioxide and water in the lungs.
The CO2 is then exhaled and only water remains.
TABLE 8.2 Buffering Capacity of Blood Components
Buffer
Slykesa
%
Bicarbonate
Hemoglobin
Proteins
Phosphates
18.0
8.0
1.7
0.3
64
29
6
1
Total
28.0
100
aMilliequivalents
of hydrogen ions taken up by each liter of blood from pH 7.4 to 7.0.
494
The amount of bicarbonate that combines with H+ equals the
amount of acid buffered. When lactic acid decreases the blood’s pH
from 7.4 to 7.0, more than 60% of the bicarbonate initially present in
the blood has been used. Even under resting conditions, the acid
produced by the end products of metabolism would use up a major
portion of the bicarbonate from the blood if there were no other way
of removing H+ from the body. Blood and chemical buffers are
required only to transport metabolic acids from their sites of
production (the muscles) to the lungs or kidneys, where they can be
removed. Once H+ is transported and removed, the buffer molecules
can be reused.
In the muscle fibers and the kidney tubules, H+ is primarily buffered
by phosphates, such as phosphoric acid and sodium phosphate. Less
is known about the capacity of the buffers intracellularly, although
cells contain more protein and phosphates and less bicarbonate than
do the extracellular fluids.
As noted earlier, any increase in free H+ in the blood stimulates the
respiratory center to increase ventilation. This facilitates the binding
of H+ to bicarbonate and the removal of carbon dioxide. The end
result is a decrease in free H+ and an increase in blood pH. Thus,
both the chemical buffers and the respiratory system provide shortterm means of neutralizing the acute effects of exercise acidosis. To
maintain a constant buffer reserve, the accumulated H+ is removed
from the body via excretion by the kidneys and eliminated in urine.
The kidneys filter H+ from the blood along with other waste products.
This provides a way to eliminate H+ from the body while maintaining
the concentration of extracellular bicarbonate.
495
During sprint exercise, muscle glycolysis generates a large amount
of lactate and H+, which lowers the muscle pH from a resting level of
7.1 to less than 6.7. As shown in table 8.3, an all-out 400 m sprint
decreases leg muscle pH to 6.63 and increases muscle lactate from a
resting value of 1.2 mmol/kg to almost 20 mmol/kg of muscle. Such
disturbances in acid–base balance can impair muscle contractility
and its capacity to generate adenosine triphosphate (ATP). Lactate
and H+ accumulate in the muscle, in part because they do not freely
diffuse across the skeletal muscle fiber membranes. Despite the great
production of lactate and H+ during the ~60 s required to run 400 m,
these by-products diffuse throughout the body fluids and reach
equilibrium after only about 5 to 10 min of recovery. Five minutes after
the exercise, the runners described in table 8.3 had blood pH values
of 7.10 and blood lactate concentrations of 12.3 mmol/L, compared
with a resting pH of 7.40 and a resting lactate level of 1.5 mmol/L.
496
FIGURE 8.18 Effects of active and passive recovery on blood lactate concentrations after a series of
exhaustive sprint bouts. Note that the blood lactate removal rate is faster when the subjects perform
exercise during recovery than when they rest during recovery.
Reestablishing normal resting concentrations of blood and muscle
lactate after such an exhaustive exercise bout is a relatively slow
process, often requiring 1 to 2 h. As shown in figure 8.18, recovery of
blood lactate to the resting level is facilitated by continued lowerintensity exercise, called active recovery.3 After a series of exhaustive
sprint bouts, the participants in this study either sat quietly (passive
recovery) or exercised at an intensity of 50% O2max. Blood lactate is
removed more quickly during active recovery because the activity
maintains elevated blood flow through the active muscles, which in
turn enhances both lactate diffusion out of the muscles and lactate
oxidation.
Although blood lactate remains elevated for 1 to 2 h after highly
anaerobic exercise, blood and muscle H+ concentrations return to
normal within 40 min of recovery. Chemical buffering, principally by
bicarbonate, and respiratory removal of excess carbon dioxide are
responsible for this relatively rapid return to normal acid–base
homeostasis.
In Review
Excess H+ (decreased pH) impairs muscle contractility and ATP generation.
497
The respiratory and renal systems play integral roles in maintaining acid–base
balance. The renal system is involved in more long-term maintenance of acid–
base balance through the secretion of H+.
Whenever H+ concentration starts to increase, the inspiratory center responds by
increasing the rate and depth of respiration. Removing carbon dioxide is an
essential means of reducing H+ concentrations.
Carbon dioxide is transported in the blood primarily bound to bicarbonate. Once it
reaches the lungs, carbon dioxide is formed again and exhaled.
Whenever H+ concentration begins to increase, whether from carbon dioxide or
lactate accumulation, bicarbonate ion can buffer the H+ to prevent acidosis.
498
IN CLOSING
In this chapter, we discussed the responses of the cardiovascular and
respiratory systems to exercise. We also considered the limitations that these
systems can impose on abilities to perform sustained aerobic exercise. The next
chapter presents basic principles of exercise training, allowing us to better
understand in the subsequent chapters how the body adapts to resistance
training as well as aerobic and anaerobic training.
KEY TERMS
afterload
anaerobic threshold
cardiovascular drift
central command
dyspnea
exercise-induced arterial hypoxemia (EIAH)
Frank-Starling mechanism
hydrostatic pressure
hyperventilation
maximal voluntary ventilation
maximum heart rate (HRmax)
oncotic pressure
preload
rate–pressure product (RPP)
resting heart rate (RHR)
steady-state heart rate
total peripheral resistance (TPR)
Valsalva maneuver
ventilatory equivalent for carbon dioxide (
ventilatory equivalent for oxygen (
ventilatory threshold
/ CO2)
E
/ O2)
E
STUDY QUESTIONS
1.
Describe how heart rate, stroke volume, and cardiac output respond to
increasing rates of work. Illustrate how these three variables are
interrelated.
2.
How do we determine HRmax? What are alternative methods using indirect
estimates? What are the major limitations of these indirect estimates?
3.
What information can be learned from measuring heart rate variability?
499
4.
Describe two important mechanisms for returning blood back to the heart
during exercise in an upright position.
5.
Explain why the ability to increase stroke volume is important in determining
maximal oxygen consumption.
6.
What is the Fick principle, and how does this apply to our understanding of
the relationship between metabolism and cardiovascular function?
7.
8.
9.
Define the Frank-Starling mechanism. How does this work during exercise?
10.
What is cardiovascular drift? What two theories have been proposed to
explain this phenomenon?
11.
What changes occur in the plasma volume and red blood cells with
increasing levels of exercise? With prolonged exercise in the heat?
12.
How does pulmonary ventilation respond to increasing intensities of
exercise?
13.
Define the terms dyspnea, hyperventilation, Valsalva maneuver, and
ventilatory threshold.
14.
What causes exercise-induced asthma in some athletes? What athletes are
most prone to being affected?
15.
16.
What role does the respiratory system play in acid–base balance?
17.
What are the primary buffers in the blood? In muscles?
How does blood pressure respond to exercise?
What are the major cardiovascular adjustments that the body makes when
someone is overheated during exercise?
What is the normal resting pH for arterial blood? For muscle? How are
these values changed as a result of exhaustive sprint exercise?
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
500
PART III
Exercise Training
The study of exercise physiology relies heavily on the understanding
of (1) how the body responds during acute bouts of exercise and (2)
how it adapts to repeated exercise sessions (i.e., training
responses). In the two previous sections of the book, we examined
the control and function of skeletal muscle during acute exercise
(part I) and the roles of the cardiovascular and respiratory systems in
supporting those functions (part II). In part III, we examine how these
systems adapt when exposed to repeated bouts of exercise (i.e.,
adaptations to training). Chapter 9, Principles of Exercise Training,
lays the groundwork for subsequent chapters by discussing the
terminology and training principles used by exercise physiologists.
The principles presented in this chapter can be used to optimize the
physiological adaptations to a training program. In chapter 10,
Adaptations to Resistance Training, we consider the mechanisms
through which muscular strength and muscular endurance improve
in response to resistance training. Finally, in chapter 11, Adaptations
to Aerobic and Anaerobic Training, we discuss the changes in
various systems of the body that result from performing regular
physical activity involving a wide variety of combinations of exercise
intensity and duration. Training adaptations that ultimately lead to
improvements in exercise capacity and athletic performance are
specific to all aspects of the training to which those physiological
systems are exposed.
501
502
503
9
Principles of Exercise Training
In this chapter and in the web study guide
Terminology
Muscular Strength
Muscular Power
Muscular Endurance
Aerobic Power
Anaerobic Power
ACTIVITY 9.1 Basic Training Principles reviews the basic training principles and connects them to a
real-life situation.
General Principles of Training
Principle of Individuality
Principle of Specificity
Principle of Reversibility
Principle of Progressive Overload
Principle of Variation
Resistance Training Programs
Recommendations for Resistance Training Programs
Types of Resistance Training
AUDIO FOR FIGURE 9.4 explains what happens in the muscle during box jumping.
ACTIVITY 9.2 Forms of Resistance Training explores the characteristics of the different forms of
resistance training.
Anaerobic and Aerobic Power Training Programs
Group Exercise Training
Interval Training
Continuous Training
Interval-Circuit Training
High-Intensity Interval Training (HIIT)
504
ACTIVITY 9.3 Evaluating an Aerobic Training Program provides an opportunity to evaluate a basic
aerobic power training program.
AUDIO FOR FIGURE 9.6 describes interval training at three different intensities for training each energy
system.
In Closing
505
A
merican Ashton Eaton won the gold medal in the decathlon at the 2012
Olympic Games in London, accumulating 8,869 points over the grueling 2-day
competition. At the U.S. Olympic Trials in June of that year, Eaton had broken the
9,000-point barrier as well as the world record, previously held by Roman Šebrle of
the Czech Republic, whose mark had stood for 11 years. Decathletes are
considered by many to be the ultimate athletes, since they have to compete in
events that test their speed, strength, power, agility, and endurance. The decathlon
is a 2-day event made up of the 100 m sprint, long jump, shot put, high jump, and
400 m run on the first day, and the 110 m hurdles, discus, pole vault, javelin, and
1,500 m run on the second day. Because training is very specific to the sport or
event, intense muscular power training to increase the distance one can heave a 16
lb (~7 kg) shot put does little to improve one’s 1,500 m run time. Decathletes spend
countless hours training specifically for each of their 10 events, fine-tuning their
training techniques to maximize performance in each event.
Previous chapters examining the acute response to exercise covered
the body’s immediate response to a single exercise bout. We now
investigate how the body responds to repeated bouts of exercise
performed over a period of time—exercise training. When one
performs regular exercise over a period of days, weeks, and months,
a variety of physiological adaptations occur. The positive adaptations
that accompany proper training principles lead to improvement in
both exercise capacity and sport performance. With resistance
training, muscles become stronger. With aerobic training, the heart
and lungs become more efficient at oxygen delivery, and exercise
endurance increases. With high-intensity anaerobic training, the
neuromuscular, metabolic, and cardiovascular systems adapt to
generate more adenosine triphosphate (ATP) per unit of time, thus
increasing muscular endurance and speed of movement over short
periods of time. These adaptations are highly specific to the type of
training performed. Before examining specific adaptations to training,
this chapter first looks at the basic terminology and general principles
used in exercise training and then gives an overview of the elements
of proper training programs.
506
Terminology
Before discussing the principles of exercise training, we first define
key terms that will be used throughout the rest of this book.
Muscular Strength
Strength is defined as the maximal force that a muscle or muscle
group can generate. Someone with a maximal capacity to bench
press 100 kg (220 lb) has twice the strength of someone who can
bench press 50 kg (110 lb). In this example, strength is defined as the
maximal weight the individual can lift with one single effort. This is
referred to as 1-repetition maximum (1RM). To determine 1RM in
the weight room or fitness center, people select a weight that they
know they can lift at least one time. After a proper warm-up, they try
to execute several repetitions. If they can perform more than one
repetition, they add weight and try again to execute several
repetitions. This continues until the person is unable to lift the weight
more than a single repetition. This last weight that can be lifted only
once is the 1RM for that particular exercise. The 1RM is commonly
used in the laboratory or weight room as a measure of strength.
Muscular strength can also be accurately measured in the
research laboratory through use of specialized equipment that allows
quantification of static strength and dynamic strength at various
speeds and at various angles in the joint’s range of motion (see figure
9.1). Gains in muscular strength involve changes in both the structure
of the muscle and its neural control. These are discussed in chapter
10.
507
FIGURE 9.1 An isokinetic testing and training device.
Muscular Power
Power is defined as the rate at which work is performed, thus the
product of force and velocity. Unlike strength, it has a speed
component. Maximal muscular power, generally referred to simply as
power, is the explosive aspect of strength, the product of strength and
the velocity of movement.
Power = force × distance / time,
where force = strength
and distance / time = velocity
508
Consider an example. Two individuals can each bench press 200
kg (441 lb), moving the weight the same distance, from where the bar
touches the chest to full extension of the arms. But the person who
can do it in 1 s has twice the power of the individual who takes 2 s to
perform the lift. This is illustrated in table 9.1.
Although absolute strength is an important component of
performance, muscular power is the functional application of both
strength and speed of movement. It is a key component in almost
every sport and competitive activity. In football, for example, an
offensive lineman with a bench press 1RM of 200 kg (441 lb) may be
unable to control a defensive lineman with a bench press 1RM of only
150 kg (330 lb) if the defensive lineman can move his 1RM at a much
faster speed. The offensive lineman is 50 kg (110 lb) stronger, but the
defensive lineman’s faster speed coupled with adequate strength
could give him the performance edge. Although simple field tests are
available to estimate power, these tests are generally not very
specific to power because their results are affected by other factors.
Power can be measured, however, through use of more sophisticated
electronic devices, such as the one depicted in figure 9.1.
Throughout this book, the primary concern is with issues of
muscular strength, with only brief mention of muscular power. Recall
that power has two components: strength and speed. Speed is a
more innate quality that changes little with training. Thus,
improvements in power follow improvements in strength gained
through traditional resistance training programs. However, high power
output exercises, such as vertical jump training and some types of
resistance training, have been shown to increase power for those
specific movements.1
Muscular Endurance
Many sporting activities depend on the muscles’ ability to repeatedly
develop or sustain submaximal forces or to do both. The capacity to
perform repeated muscle contractions, or to sustain a contraction
over time, is termed muscular endurance. Examples of muscular
endurance include performing sit-ups or push-ups or sustaining force
in an attempt to pin an opponent in wrestling. Although several valid
laboratory techniques are available to directly measure muscular
endurance, a simple way to estimate it is to assess the maximum
509
number of repetitions one can perform at a given percentage of 1RM.
For example, a man who has a 1RM for the bench press of 100 kg
(220 lb) could evaluate his muscular endurance independent of his
muscular strength by measuring how many repetitions he could
perform at, for example, 75% of that 1RM (75 kg, or 165 lb). Muscular
endurance is increased through gains in muscular strength and
through changes in local blood flow and metabolic function. Metabolic
and circulatory adaptations that occur with training are discussed in
chapter 11.
TABLE 9.1 Strength, Power, and Muscular Endurance of
Three Athletes Performing the Bench Press
Component
Athlete A
Athlete B
Athlete C
Strengtha
Powerb
100 kg
100 kg lifted 0.6 m in 0.5 s
= 120 kg · m/s
= 1,177 J/s or 1,177 W
10 repetitions with 75 kg
200 kg
200 kg lifted 0.6 m in 2.0 s
= 60 kg · m/s
= 588 J/s or 588 W
10 repetitions with 150 kg
200 kg
200 kg lifted 0.6 m in 1.0 s
= 120 kg · m/s
= 1,177 J/s or 1,177 W
5 repetitions with 150 kg
Muscular endurancec
aStrength
was determined by the maximum amount of weight the athlete could bench press just once (i.e., the 1RM).
was determined as the athlete performed the 1-repetition maximum (1RM) test as explosively as possible. Power was
calculated as the product of force (weight lifted) times the distance lifted from the chest to full arm extension (0.6 m, or about 2 ft),
divided by the time it took to complete the lift.
cMuscular endurance was determined by the greatest number of repetitions that could be completed using 75% of the 1RM.
bPower
Table 9.1 illustrates the functional differences between strength,
power, and muscular endurance in three athletes. The actual values
have been exaggerated for the purpose of illustration. From this table
we can see that although athlete A has half the strength of athletes B
and C, he has twice the power of athlete B and is equal in power to
athlete C. Therefore, because of his fast speed of movement, his lack
of strength does not seriously limit his power output. Also, for
purposes of designing training programs, the analysis of these three
athletes indicates that athlete A should focus training on developing
strength, without losing speed; athlete B should focus on training
explosively to improve speed of movement (although this is unlikely
to change much); and athlete C should focus training on developing
muscular endurance. These recommendations are made assuming
that each athlete needs to optimize performance in each of these
three areas.
Aerobic Power
510
Aerobic power is defined as the rate of energy release by cellular
metabolic processes that depend on the continued availability of
oxygen. It is synonymous with the terms aerobic capacity and
maximal oxygen uptake ( O2max). Maximal aerobic power is the
highest oxygen uptake that an individual can obtain during dynamic
exercise using large muscle groups for a few minutes. It depends on
the maximal capacity for aerobic resynthesis of ATP. In most healthy
individuals, maximal aerobic power is limited primarily by the central
cardiovascular system and to a lesser extent by respiration and
metabolism. The best laboratory test of aerobic power is a graded
exercise test to exhaustion during which O2 is measured and
O2max is determined, as discussed in detail in chapter 5. A number of
field tests, most often measuring the time needed to walk or run a set
distance, or the distance covered in a given time, have been
developed to estimate O2max without the need to actually measure it
in the laboratory.
Anaerobic Power
Anaerobic power is defined as the rate of energy release by cellular
metabolic processes that function without the involvement of oxygen.
Maximal anaerobic power, or anaerobic capacity, is defined as the
maximal capacity of the anaerobic systems (ATP-phosphocreatine
[PCr] system and anaerobic glycolytic system) to produce ATP. Unlike
the situation with aerobic power, there is no universally accepted
laboratory test to determine anaerobic power. Several tests provide
estimates of maximal anaerobic power, including the maximal
accumulated oxygen deficit test, the critical power test, and the
Wingate anaerobic test.
The commonly used Wingate test involves 30 s of all-out pedaling
against a constant resistance on a cycle ergometer. The resistance,
or braking force, is determined by the person’s weight, sex, age, and
level of training. Given a 5 s countdown, subjects begin to pedal as
fast as they can, and the resistance is increased instantaneously and
held constant for the duration of the test. Peak anaerobic power is
determined from the number of revolutions performed in the first 5 s,
while anaerobic capacity is measured as the total work performed
during the 30 s.
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In Review
Muscular strength refers to the ability of a muscle or muscle group to exert force.
Muscular power is the rate of performing work, or the product of force and
velocity.
Muscular endurance is the capacity to sustain a static contraction or to perform
repeated muscle contractions.
Maximal aerobic power, or aerobic capacity, is the highest oxygen uptake that an
individual can obtain during sustained dynamic exercise using large muscle
groups.
Maximal anaerobic power, or anaerobic capacity, is defined as the maximal
capacity of the anaerobic energy systems to produce ATP.
General Principles of Training
Chapters 10 and 11 present in detail the specific physiological
adaptations that result from resistance training, aerobic training, and
anaerobic training. Several principles, however, apply to all forms of
exercise training.
Principle of Individuality
Individuals do not all possess the same inherent ability to respond to
an acute exercise bout or the same capacity to adapt to exercise
training. Heredity plays a major role in determining the body’s
response to a single bout of exercise, as well as the chronic changes
that result from a training program. This is the principle of
individuality. Except for identical twins, no two people have exactly
the same genetic characteristics, so individuals are unlikely to exhibit
the same responses. Variations in cellular growth rates, metabolism,
cardiovascular and respiratory regulation, and neural and endocrine
regulation lead to tremendous individual variation. Such individual
variation likely explains why some people show great improvement
after participating in a given program (“high responders”) whereas
others experience little or no change after following the same
program (“low responders”). We discuss this phenomenon of high
and low responders in more detail in chapter 11. For these reasons,
any training program must take into account the specific needs and
abilities of the individuals for whom it is designed. Do not expect all
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individuals to have exactly the same degree of improvement, even
when they train exactly the same.
Principle of Specificity
Training adaptations are highly specific to the type of activity being
performed and to the volume and intensity of the exercise. To
improve muscular power, for example, a shot-putter would not
emphasize distance running or slow, low-intensity resistance training.
The shot-putter needs to develop explosive power. Similarly, the
marathon runner would not focus on sprint training. This is likely the
reason that athletes who train for strength and power, such as
weightlifters, often have great strength but don’t have highly
developed aerobic endurance when compared to untrained people.
According to the principle of specificity, exercise adaptations are
specific to the mode, intensity, and duration of training, and the
training program must stress the physiological systems that are
critical for optimal performance in a given sport in order to achieve
specific training adaptations and goals.
Principle of Reversibility
Resistance training improves muscle strength and the capacity to
resist fatigue. Likewise, endurance training improves the ability to
perform aerobic exercise at higher intensities and for longer periods.
But if training is decreased or stopped (detraining), the physiological
adaptations that caused those improvements in performance will be
reversed. Any gains achieved with training will eventually be lost. The
principle of reversibility lends scientific support to the saying “Use it
or lose it.” All effective training programs must include a maintenance
plan that sustains the physiological adaptations gained by training. In
chapter 14, we examine specific physiological changes that occur
when the training stimulus stops.
RESEARCH PERSPECTIVE 9.1
Can Aerobic Exercise Increase Muscle Size?
The principle of specificity states that training adaptations are highly specific to
the type of training performed. Aerobic exercise training is associated with
improvements in aerobic capacity and cardiorespiratory function. However,
there is debate among exercise physiologists about the impact of aerobic
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exercise training on skeletal muscle mass. Historically, it has been assumed
that aerobic exercise has little effect on skeletal muscle hypertrophy. With the
development of high-resolution imaging techniques, accumulating evidence
now suggests that aerobic exercise training can improve muscle mass in
sedentary individuals across the life span. The first of these studies
established that 6 months of walking or running training could increase the
cross-sectional area of the thigh by 9% in older men.13 In that study, while the
older men experienced a robust increase in muscle size, a group of young
men did not show any changes in muscle size with the training. (This result
may have been because the younger men attended fewer exercise sessions
than the older men did throughout the study. The effectiveness of aerobic
exercising training to induce skeletal muscle hypertrophy likely depends on
obtaining sufficient exercise intensities, duration, and frequency to accumulate
a large number of muscle contractions at this lower load.) Studies that have
compared aerobic training with resistance training have found that, on
average, both modalities increase muscle size by approximately the same
percentage (~7%-9%) from baseline.
Aside from just increasing whole muscle size, aerobic training increased
slow- and fast-twitch myofiber cross-sectional area of the exercised muscle in
the majority of studies. Similarly, studies of the metabolic turnover of muscle
proteins showed that aerobic exercise acutely and chronically stimulated
skeletal muscle protein synthesis, resulting in a positive muscle protein
balance and increased myofiber size, even in older men and women who
might otherwise have age-related anabolic impairments. Despite a lack of
standard methodology to measure muscle protein breakdown, most studies
examining muscle protein breakdown and aerobic training agree that aerobic
training results in reduced catabolic factors, leading to skeletal muscle
hypertrophy.
Overall, the existing research indicates that aerobic exercise training can
produce skeletal muscle hypertrophy.11 Aerobic exercise-induced changes in
the molecular regulation and protein metabolism of skeletal muscle increase
both individual myofiber and whole muscle size in sedentary individuals.
These data show that aerobic exercise should be acknowledged for its ability
to increase skeletal muscle mass and considered an effective countermeasure
for age-related muscle atrophy.
Principle of Progressive Overload
Two important concepts, overload and progressive training, form the
foundation of all training programs. According to the principle of
progressive overload, systematically increasing the demands on the
body is necessary for continued improvement. For example, when
undergoing a strength training program, in order to gain strength the
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muscles must be overloaded, which means they must be loaded
beyond the point to which they are normally loaded. Progressive
resistance training implies that as the muscles become stronger,
either increased resistance or increased repetitions or both are
required to stimulate further strength increases.
As an example, consider a young woman who can perform only 10
repetitions of a bench press before reaching fatigue, using 30 kg (66
lb) of weight. With a week or two of resistance training, she should be
able to increase to 14 or 15 repetitions with the same weight. She
then adds 2.3 kg (5 lb) to the bar, and her repetitions decrease to 8 or
10. As she continues to train, the repetitions continue to increase,
and within another week or two, she is ready to add another 2.3 kg of
weight. Thus, improvement depends on a progressive increase in the
amount of weight lifted. In a similar way, training volume (intensity
and duration) must be increased progressively with anaerobic and
aerobic training for further improvements to occur.
Principle of Variation
The principle of variation, also called the principle of
periodization, first proposed in the 1960s, has become very popular
in the area of resistance training. Periodization is the systematic
process of changing one or more variables in the training program—
mode, volume, or intensity—over time to allow for the training
stimulus to remain challenging and effective.1 Training intensity and
volume of training are the most commonly manipulated aspects of
training to achieve peak levels of fitness for competition. Classical
periodization involves high initial training volume with low intensity;
then, as training progresses, volume decreases and intensity
gradually increases. Undulating periodization uses more frequent
variation within a training cycle.
For sport-specific training, the volume and intensity of training are
varied over a macrocycle, which is generally up to a year of training.
A macrocycle is composed of two or more mesocycles that are
dictated by the dates of major competitions. Each mesocycle is
subdivided into periods of preparation, competition, and transition.
This principle is discussed in greater detail in chapter 14.
In Review
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According to the principle of individuality, each person responds uniquely to
training, and training programs must be designed to allow for individual variation.
According to the principle of specificity, to maximize benefits, training must be
specifically matched to the type of activity or sport the person engages in. An
athlete involved in a sport that requires tremendous strength, such as
weightlifting, would not expect great strength gains from endurance running.
According to the principle of reversibility, training benefits are lost if training is
either discontinued or reduced abruptly. To avoid this, all training programs must
include a maintenance program.
According to the principle of progressive overload, as the body adapts to training
at a given volume and intensity, the stress placed on the body must be increased
progressively for the training stimulus to remain effective in producing further
improvements.
According to the principle of variation (or periodization), one or more aspects of
the training program should be altered over time to maximize effectiveness of
training. The systematic variation of volume and intensity is most effective for
long-term progression.
Resistance Training Programs
Over the past 75 years, research has provided a substantial
knowledge base concerning resistance training and its application to
health and sport. The health aspects of resistance training are
discussed in chapter 20. This section concerns primarily the use of
resistance training for sport.
Recommendations for Resistance Training Programs
Resistance training programs can be designed and prescribed in
terms of
the exercises that will be performed;
the order in which they will be performed;
the number of sets for each exercise;
the rest periods between sets and between exercises; and
the amount of resistance, the number of repetitions, and the
velocity of movement to be used.
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In 2009, the American College of Sports Medicine (ACSM) revised its
position stand on progressive resistance training for healthy adults
(table 9.2).1 Previous statements specified, for all adults, a minimum
of one set of 8 to 12 reps for each of 8 to 10 different exercises that
together involve all of the major muscle groups. The new position
stand recommends resistance training models specific to desired
outcomes, that is, improvements in strength, muscle hypertrophy,
power, local muscular endurance, or gross motor performance.
Resistance programs aimed at improving strength should involve
repetitions with both concentric (muscle shortening) and eccentric
(muscle lengthening) actions. Isometric contractions play a beneficial,
but secondary, role and may be included as well. Concentric strength
improvement is greatest when eccentric exercises are included, and
eccentric training has been shown to produce specific benefits for
those action-specific movements. Large muscle groups should be
stressed before smaller groups, multiple-joint exercises before singlejoint exercises, and higher-intensity efforts before those of lower
intensity. Table 9.2 provides a summary of the ACSM
recommendations on loading, volume (sets and reps), velocity of
movements, and frequency of training.
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It is recommended that rest periods of 2 to 3 min or more be used
between heavy loads for novice and intermediate lifters; for advanced
lifters, 1 or 2 min may suffice. Once an individual can perform the
current workload at or above the desired number of reps for two
consecutive training sessions, a 2% to 10% increase in load should
be applied. While both machine-based exercises and free weights
can be used for novice and intermediate lifters, for advanced lifters,
the emphasis should be placed on free weights.
When muscle hypertrophy (in bodybuilders, for example) or
development of muscular power is the goal, recommendations for
sequencing, rest periods, and so on are the same as those for
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strength development. However, as shown in table 9.2, other aspects
of the program differ.
Types of Resistance Training
Resistance training can use static contractions, dynamic contractions,
or both. Dynamic contractions can include concentric or eccentric
contractions, or both. Typical resistance training can be performed
using free weights, variable-resistance devices, isokinetic devices,
and plyometrics.
Static-Contraction Resistance Training
Static-contraction resistance training, also called isometric
training, gained great popularity in the mid-1950s as a result of
research by several German scientists. These studies indicated that
static resistance training caused tremendous strength gains and that
those gains exceeded the gains resulting from dynamic-contraction
procedures. Subsequent studies were unable to reproduce the
original studies’ results, and training programs based heavily on
isometric contractions have generally fallen out of favor. However,
static contractions remain an important form of training, particularly
for core stabilization (discussed later in the chapter) and for
enhancing grip strength.1 Additionally, in postsurgical rehabilitation
when a limb is immobilized and thus incapable of dynamic
contractions, static contractions facilitate recovery and reduce muscle
atrophy and strength loss.
Free Weights Versus Machines
With free weights, such as barbells and dumbbells, the resistance or
weight lifted remains constant throughout the dynamic range of
movement. If a 50 kg (110 lb) weight is lifted, it will always weigh 50
kg. In contrast, a variable-resistance contraction involves varying the
resistance to try to match it to the strength curve. Figure 9.2
illustrates how strength varies throughout the range of motion in a
two-arm curl. Maximal strength production by the elbow flexors
occurs at approximately 100° in the range of movement. These
muscles are weakest at 60° (elbows fully flexed) and at 180° (elbows
fully extended). In these positions, one is able to generate only 67%
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and 71%, respectively, of the maximal force-producing capabilities at
the optimal angle of 100°.
FIGURE 9.2 The variation in strength relative to the angle of the elbow during the two-arm curl.
Strength is optimized at an angle of 100°. The maximal force-development capacity of the muscle group
at a given angle is given as a percentage of the capacity at the optimal angle of 100°.
When one is using free weights, the range of motion is less
restricted than with machines, and the resistance or weight used to
train the muscle is limited by the weakest point in that range of
motion. If the person in figure 9.2 had the capacity to lift only 45 kg
(100 lb) at the optimal angle of 100°, then he would be able to lift only
32 kg (71 lb) at the fully extended position of 180°. Therefore, if he is
starting with a barbell loaded with 32 kg, he can just barely move it
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from the fully extended position to start his lift. However, by the time
he gets to an angle of 100° in his full range of motion, he is lifting only
70% of what he could maximally lift at that angle. Thus, free weights
maximally tax the weakest points in the range of motion and provide
moderate resistance at the midrange (90°-140°). Individuals
performing the two-arm curl tend to greatly reduce their range of
motion as they start to fatigue (referred to as “cheating”). They are
simply trying to stay out of the weakest portion of their range of
motion. The bottom line is that with free weights, the maximum weight
one can lift is limited by the weakest portion in the range of motion,
which means that the strongest position in the range of motion is
never maximally taxed! However, free weights do offer some distinct
advantages, especially for the expert lifter.
Starting in the 1970s, a number of resistance training machines or
devices were introduced that used stacked weights, variableresistance, and isokinetic techniques. Variable-resistance machines
use cams, pulleys, and levers to vary the weight throughout the range
of movement. Such machines have been regarded as safer; they are
easy to use and allow performance of some exercises that are difficult
to do with free weights. Machines help stabilize the body, especially
for novice lifters, and limit the muscle action to that desired without
extraneous muscle groups firing.
On the other hand, free weights offer some advantages that
resistance machines do not provide. The lifter must control the weight
being lifted. A lifter must recruit more motor units—not only in the
muscles being trained but also in supporting muscles—to gain control
of the bar, stabilize the weight lifted, and maintain body balance. The
lifter must both balance and stabilize the weight. In that regard, when
an athlete is training for a sport such as football, the experience with
free weights more closely resembles actions associated with actual
sport competition. Also, because free weights do not limit the range of
motion of a particular exercise, optimal training specificity can be
achieved. Whereas a bicep curl on a machine may be done only in
the vertical plane, an athlete using free weights can perform the curl
in any plane, choosing one, for example, that reflects a sport-specific
motion. And finally, data show that if significant strength gains are to
521
be achieved over a shortened training period, free weights may
provide greater strength gains than many types of weight machines.
Both machine-based resistance programs and free-weight training
programs result in measurable gains in strength, hypertrophy, and
power. Free-weight programs result in greater improvements in freeweight tests, and machine training results in greater gains in
machine-based tests. The choice to use weight machines versus free
weights depends on the experience of the lifter and the desired
outcomes.
Eccentric Training
Another form of dynamic-contraction resistance training, called
eccentric training, emphasizes the eccentric phase. With eccentric
contractions, the muscle’s ability to resist force is considerably
greater than with concentric contractions (see chapter 1). Subjecting
the muscle to this greater training stimulus theoretically produces
greater strength gains. A number of studies have shown the
importance of including the eccentric phase of muscle contraction
along with the concentric phase to maximize gains in muscle strength
and size. Further, eccentric contraction is important to stimulate
muscle hypertrophy, as discussed in the next chapter.
Variable-Resistance Training
With a variable-resistance device, the resistance is decreased at the
weakest points in the range of movement and increased at the
strongest points. Variable-resistance training is the basis for
several popular resistance training machines. The underlying theory
is that the muscle can be more fully trained if it is forced to act at
higher constant percentages of its capacity throughout each point in
its range of movement. Figure 9.3 illustrates a variable-resistance
device in which a cam alters the resistance through the range of
motion. As noted earlier, there are advantages and disadvantages to
training using such machines.
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FIGURE 9.3 A variable-resistance training device that uses a cam to alter the resistance through the
range of motion.
Isokinetic Training
Isokinetic training is conducted with equipment that keeps
movement speed constant. Whether one applies very light force or an
all-out maximal muscle contraction, the speed of movement does not
vary. Using electronics, air, or hydraulics, the device can be preset to
control the speed of movement (angular velocity) from 0°/s (static
contraction) to 300°/s or higher. An isokinetic device is illustrated in
figure 9.1. Theoretically, if properly motivated, the individual can
contract the muscles at maximal force at all points in the range of
motion.
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Plyometrics
Plyometrics, or stretch–shortening cycle exercise, became popular
during the late 1970s and early 1980s, primarily for improving
jumping ability. As an example, to develop knee extensor muscle
strength and power, a person goes from standing upright to a deep
squat position (eccentric contraction) and then jumps up onto a box
(concentric contraction), landing in a squat position on top of the box.
The person then jumps off the box onto the ground, landing in a squat
position, and repeats the sequence with the next box (see figure 9.4).
Proposed to bridge the gap between speed and strength training,
plyometrics uses the stretch reflex to facilitate recruitment of motor
units. It also stores energy in the elastic and contractile components
of muscle during the eccentric contraction (stretch) that can be
recovered during the concentric contraction.
Electrical Stimulation
One can stimulate a muscle by passing an electric current directly
across it or its motor nerve. This technique, called electrical
stimulation, has proven effective in clinical settings to reduce the
loss of strength and muscle size during periods of immobilization and
to restore strength and size during rehabilitation. Electrical stimulation
training also has been used experimentally in healthy subjects
(including athletes). Athletes have used this technique to supplement
their regular training programs, but no evidence shows any additional
gains in strength, power, or performance from this supplementation.
Core Training
In recent years, a significant emphasis has been placed on core
stability and strengthening exercises. While there are varying
opinions on what anatomical features constitute the core, the general
consensus is that the core is the group of trunk muscles that surround
the spine and abdominal viscera and include the abdominal, gluteal,
hip girdle, paraspinal, and other accessory muscles.
Initially, this type of core-specific exercise training was explored in
rehabilitation settings, specifically for the treatment of lower back
pain, but its benefits have also been recognized in sport performance.
Theoretically, greater core stability could benefit sport performance by
providing a foundation for greater force production and force transfer
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to the extremities. For example, having the core stabilized and
engaged in the simple action of throwing a ball allows for greater
biomechanical efficiency in the limb transmitting the force to throw the
ball and for the activation of stabilizing muscles in the contralateral
arm. The principle of core stabilization promotes proximal stability for
distal mobility.
FIGURE 9.4 Plyometric box jumping (see the text for a detailed explanation).
There has been little definitive research on the benefits of core
stability and core strengthening for athletic performance. One reason
is that there are no standardized tests for evaluating core strength
and stability. Further, the studies that have been done have been
mainly with injured populations and not specific to athletic
performance. However, the limited research does show that this type
of training decreases the likelihood of injury, especially in the lower
back and the lower extremities, during sport performance. The
physiological explanation for this finding is that core stability training
increases the sensitivity of the muscle spindles, thereby permitting a
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greater state of readiness for loading joints during movement15 and
protecting the body from injury.
The many different types of core stability and strengthening
training include balance and instability resistance (e.g., physioball). It
is thought that because the core is composed mainly of type I muscle
fibers, the core musculature may respond well to multiple sets of
exercises with high repetitions.4 Yoga, Pilates, tai chi, and the
physioball are commonly incorporated into athletes’ training programs
to promote core stability and strength. Further research is needed to
determine the benefits of core training and the underlying
mechanisms.
In Review
Low-repetition, high-resistance training enhances strength development, whereas
high-repetition, low-intensity training optimizes the development of muscular
endurance.
Variation (or periodization), through which various aspects of the training program
are altered, is important to optimize results and prevent overtraining or burnout.
Resistance programs aimed at improving strength should involve repetitions with
both concentric (muscle shortening) and eccentric (muscle lengthening) actions.
Isometric contractions play a beneficial, but secondary, role and may be included
as well.
Large muscle groups should be stressed before smaller groups, multiple-joint
exercises before single-joint exercises, and higher-intensity efforts before those of
lower intensity.
Rest periods of 2 to 3 min or more should be incorporated between heavy loads
for novice and intermediate lifters; for advanced lifters, 1 to 2 min may suffice.
The ability of a muscle or muscle group to generate force varies throughout the
full range of movement.
While both machine-based exercises and free weights can be used for novice and
intermediate lifters, for advanced lifters, the emphasis should be placed on free
weights.
When neutral testing devices are used, strength gains from free-weight programs
and machine-based programs are similar.
Electrical stimulation can be successfully used in rehabilitating athletes but has no
additional benefits when used to supplement resistance training in healthy
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athletes.
Exercises aimed at improving core stability may benefit sport performance by
providing a foundation for greater force production and force transfer to the
extremities while stabilizing other parts of the body. However, direct evidence of
such a benefit is lacking.
Anaerobic and Aerobic Power Training
Programs
Anaerobic and aerobic power training programs, while quite different
at the extremes (e.g., training for the 100 m dash versus the 42.2 km
[26.2 mi] full marathon), are designed along a continuum. Table 9.3
illustrates how training requirements vary in competitive running
events as one goes from short sprints to long distances. With this
table serving as an example that can be applied to all sports, the
primary emphasis for the short sprints is on training the ATP-PCr
system. For longer sprints and middle distances, the primary
emphasis is on the glycolytic system, and for the longer distances,
the primary emphasis is on the oxidative system. Anaerobic power is
represented by the ATP-PCr and anaerobic glycolytic systems, while
aerobic power is represented by the oxidative system. Note, however,
that even at the extremes, more than one energy system must be
trained.
Different types of training programs can be used to meet the
specific training requirements of each event, such as in running and
swimming, and each sport. This section describes some of the more
popular types of training programs and how they are used to improve
the specific energy systems.
Group Exercise Training
The first description of group fitness can be found in the 1968 book
Aerobics by Dr. Kenneth Cooper. His mission was to encourage
people to exercise with the goal of disease prevention rather than
disease treatment. One suggested method was a new form of
exercise that utilized dance movements, primarily from hip-hop and
jazz, choreographed with music and led by an instructor. Currently,
group fitness options focus on varying types of cardiovascular,
strength, and flexibility training. For instance, cardio classes include
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mixed martial arts, plyometric training, indoor cycling, and aquatic
activities. Multiple strength training formats exist that range from highrepetition barbell classes to boot camps with more traditional
powerlifting techniques to core-based functional actions. Finally,
flexibility is the emphasis in a range of yoga disciplines as well as in
fall or injury prevention sessions.
TABLE 9.3 Percentage of Emphasis on the Three Metabolic
Energy Systems in Training for Various Running Events
Running event
Anaerobic speed (ATPPCr system)
Anaerobic endurance (anaerobic
glycolytic system)
Aerobic endurance
(oxidative system)
100 m (109 yd)
200 m (218 yd)
400 m (436 yd)
800 m (872 yd)
1,500 m (0.93 mi)
3,000 m (1.86 mi)
5,000 m (3.10 mi)
10,000 m (6.20 mi)
Marathon (42.20 km;
26.20 mi)
95
95
80
30
20
20
10
5
5
3
2
15
65
55
40
20
15
5
2
3
5
5
25
40
70
80
90
Adapted from F. Wilt, Training for Competitive Running, in Exercise Physiology, edited by H.B. Falls (Amsterdam, Netherlands: Elsevier, 1968).
Group fitness can provide the equivalent health benefits of
independent exercise, increasing oxygen consumption, high-density
lipoprotein (HDL), and lean muscle mass while decreasing fasting
blood glucose, low-density lipoprotein (LDL), triglycerides, and fat
mass. These positive physiological results occur in parallel to the
improvement of many psychological variables such as satisfaction,
enjoyment, challenge, and motivation. Because of these health
benefits and the prevalence of many class styles, durations, and
intensities, group fitness can be an ideal recommendation for all ages
and abilities.
Interval Training
Interval training consists of repeated bouts of high- to moderateintensity exercise interspersed with periods of rest or reducedintensity exercise. Research has shown that athletes can perform a
considerably greater total volume of exercise by breaking the overall
exercise period into shorter, more intense bouts, with rest or active
recovery intervals inserted between the intense bouts.
The vocabulary used to describe an interval training program is
similar to that used in resistance training and includes the terms sets,
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repetitions, training time, training distance and frequency, exercise
interval, and rest or active recovery interval. Interval training is
frequently prescribed in these terms, as illustrated in the following
example for a middle-distance runner:
Set 1: 6 × 400 m at 75 s (90 s slow jog)
Set 2: 6 × 800 m at 180 s (200 s jog-walk)
For the first set, the athlete would run six repetitions of 400 m each,
completing the exercise interval in 75 s and recovering for 90 s
between exercise intervals with slow jogging. The second set
consists of running six repetitions of 800 m each, completing the
exercise interval in 180 s, and recovering for 200 s with walkingjogging.
While interval training is traditionally associated with track, cross
country running, and swimming, it is appropriate for all sports and
activities. One can adapt interval training procedures for each sport or
event by first selecting the form or mode of training and then
manipulating the following primary variables to fit the sport and
athlete:
Rate of the exercise interval
Distance of the exercise interval
Number of repetitions and sets during each training session
Duration of the rest or active recovery interval
Type of activity during the active recovery interval
Frequency of training per week
Exercise Interval Intensity
One can determine the intensity of the exercise interval either by
establishing a specific duration for a set distance, as illustrated in our
previous example for set 1 (i.e., 75 s for 400 m), or by using a fixed
percentage of the athlete’s maximal heart rate (HRmax). Setting a
specific duration is more practical, particularly for short sprints. One
typically determines this by using the athlete’s best time for the set
distance and then adjusting the duration according to the relative
intensity that the athlete wants to achieve, with 100% equal to the
athlete’s best time. As an example, to develop the ATP-PCr system,
the intensity should be near maximal (e.g., 90%-98%); to develop the
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anaerobic glycolytic system, it should be high (e.g., 80%-95%); and to
develop the aerobic system, it should be moderate to high (e.g.,
75%-85%). These estimated percentages are only approximations
and are dependent on the athlete’s genetic potential and fitness level,
duration of the interval (e.g., 10 s versus 10 min), number of
repetitions and sets, and duration of the active recovery interval.
FIGURE 9.5 A runner outfitted with a heart rate monitor. The receiving unit, attached to the chest strap,
picks up and transmits electrical impulses from the heart to the digital monitor and memory device worn
on the wrist. After the workout, the contents of the memory device can be downloaded to a computer.
Using a fixed percentage of the athlete’s HRmax might provide a
better index of the physiological stress experienced by the athlete.
Heart rate monitors are now readily available and relatively
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inexpensive (see figure 9.5). HRmax can be determined during a
maximal exercise test in the laboratory as described in chapter 8 or
during an all-out run on the track using the heart rate monitor.
Training the ATP-PCr system requires training at very high
percentages of the athlete’s HRmax (e.g., 90%-100%), as does training
to develop the anaerobic glycolytic system (e.g., 85%-100% HRmax).
To develop the aerobic system, the intensity should be moderate to
high (e.g., 70%-90% HRmax).
Figure 9.6 illustrates changes in blood lactate concentration in a
runner using interval training at three different intensities
corresponding to those intensities needed to train the ATP-PCr
system, the glycolytic system, and the oxidative system. The runner
performed a single set consisting of five repetitions at each intensity
on different days, and the lactate concentrations were obtained from
a blood sample taken after the last repetition of each intensity.
Monitoring blood lactate concentrations can verify the energy system
that is primarily being trained.
Distance of the Exercise Interval
The distance of the exercise interval is determined by the
requirements of the event, sport, or activity. Athletes who run or sprint
short distances, such as track sprinters, basketball players, and
soccer players, use short intervals of 30 to 200 m (33-219 yd),
although a 200 m sprinter frequently runs over distances of 300 to
400 m (328-437 yd). A 1,500 m runner may run intervals as short as
200 m to increase speed, but most of this athlete’s training would be
at distances of 400 to 1,500 m (437-1,640 yd), or even longer
distances, to increase endurance and decrease fatigue or exhaustion
in the race.
Number of Repetitions and Sets During Each Training Session
531
FIGURE 9.6 Blood lactate concentrations in a single runner following a set of five repetitions of interval
training at three different paces, each on different days, corresponding to the appropriate pace for
training each energy system.
The number of repetitions and sets is also largely determined by the
needs of the sport, event, or activity. Generally, the shorter and more
intense the interval, the greater the number of repetitions and sets
should be. As the training interval is lengthened in both distance and
duration, the number of repetitions and sets is correspondingly
reduced.
Duration of the Rest or Active Recovery Interval
The duration of the rest or active recovery interval depends on how
rapidly the athlete recovers from the exercise interval. The extent of
recovery is best determined by the reduction of the athlete’s heart
rate to a predetermined level during the rest or active recovery
period. For younger athletes (30 years of age or younger), heart rate
532
is generally allowed to drop to between 130 and 150 beats/min before
the next exercise interval begins. For those over 30 years, since
HRmax decreases ~1 beat/min per year, we subtract the difference
between the athlete’s age and 30 years from both 130 and 150. So,
for a 45-year-old, we would subtract 15 beats/min to obtain the
athlete’s recovery range of 115 to 135 beats/min. The recovery
interval between sets can be established in a similar manner, but
generally the heart rate should be below 120 beats/min.
Type of Activity During the Active Recovery Interval
The type of activity performed during the active recovery interval for
land-based training can vary from slow walking to rapid walking or
533
jogging. In the pool, slow swimming using alternative strokes or the
primary stroke is appropriate. In some cases, usually in the pool, total
rest can be used. Generally, the more intense the exercise interval,
the lighter or less intense the activity performed in the recovery
interval. As athletes become better conditioned, they are able to
increase the intensity of the exercise interval, decrease the duration
of the rest interval, or both.
Frequency of Training per Week
The frequency of training depends largely on the purpose of the
interval training. A world-class sprinter or middle-distance runner
typically works out 5 to 7 days a week, although not every workout
will include interval training. Swimmers use interval training almost
exclusively. Team sport athletes can benefit from 2 to 4 days of
interval training per week when interval training is used only as a
supplement to a general conditioning program.
Continuous Training
Continuous training involves continuous activity without rest
intervals. This can vary from long, slow distance (LSD) training to
high-intensity endurance training. Continuous training is structured
primarily to affect the oxidative and glycolytic energy systems. Highintensity continuous activity is usually performed at intensities
representing 85% to 95% of the athlete’s HRmax. For swimmers and
track and cross country athletes, this could be above, at, or near race
pace. This pace would likely match or exceed the pace associated
with the athlete’s lactate threshold. Scientific evidence has clearly
demonstrated that marathon runners typically race at, or very close
to, their lactate threshold.
Long, slow distance (LSD) training became extremely popular in
the 1960s. With this form of training, introduced in the 1920s by Dr.
Ernst van Aaken, a German physician and coach, the athlete typically
trains at relatively low intensities, between 60% and 80% of HRmax,
which is approximately the equivalent of 50% to 75% of O2max.
Distance, rather than speed, is the main objective. Distance runners
may train 15 to 30 mi (24-48 km) per day using LSD techniques, with
weekly distances of 100 to 200 mi (161-322 km). The pace of the run
is substantially slower than the runner’s maximal pace. While less
534
stressful to the cardiovascular and respiratory systems, extreme
distances can result in overuse injuries and general breakdown of
muscles and joints. Further, the serious runner needs to train at or
near race pace on a regular basis to develop leg speed and strength.
Thus, most runners vary their workout from one day to the next, from
week to week, and from month to month.
Long, slow distance training is probably the most popular and
safest form of aerobic endurance conditioning for the nonathlete who
just wants to get into shape and stay in shape for health-related
purposes. More vigorous or burst types of activity generally are not
encouraged in older, sedentary people. Long, slow distance is also a
good training program for athletes in team sports for maintaining
aerobic endurance during the season as well as the off-season.
Fartlek training, or speed play, is another form of continuous
exercise that has some components of interval training. This form of
training was developed in Sweden in the 1930s and is used primarily
by distance runners. The athlete varies the pace from high speed to
jogging speed at his or her discretion. This is a free form of training in
which fun is the primary goal, and distance and time are not even
considered. Fartlek training is normally performed in the countryside
where there are hills of various inclines. Many coaches have used
Fartlek training to supplement either high-intensity continuous training
or interval training, since it provides variety to the normal training
routine.
Interval-Circuit Training
Introduced in the Scandinavian countries in the 1960s and 1970s,
interval-circuit training combines interval and circuit training into
one workout. The circuit may be 3,000 to 10,000 m in length, with
stations every 400 to 1,600 m (437-1,750 yd). The athlete jogs, runs,
or sprints the distance between stations; stops at each station to
perform a strength, flexibility, or muscular endurance exercise in a
manner similar to that in actual circuit training; and continues on
jogging, running, or sprinting to the next station. These courses are
typically located in parks or in the country where there are many trees
and hills. Such a training regimen can benefit almost any type of
athlete and provide diversity to what might be an otherwise
monotonous training regimen.
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RESEARCH PERSPECTIVE 9.2
Tabata Training: The Original HIIT
Tabata, named for Dr. Izumi Tabata from Ritsumeikan University in Japan, is a
high-intensity interval training (HIIT) protocol that incorporates brief,
supramaximal (170% of O2max) 20 s intervals followed by 10 s of rest into a 4
min exercise bout. In 1996, Dr. Tabata published the results of a study that
found that—although just 4 min in duration—subjects who followed this HIIT
protocol 4 days a week showed notable improvements in aerobic and
anaerobic fitness, higher than those observed in subjects who performed
classical endurance training (70% of O2max) for 60 min a day.14 Subsequent
research has shown that Tabata and other HIIT programs can be effectively
used to increase aerobic and anaerobic fitness, promote fat loss, and improve
health outcomes in a relatively short period of time.12
The HIIT model of brief bouts of aerobic conditioning at close to maximal
intensity has become increasingly popular with competitive athletes to
enhance both aerobic and anaerobic endurance while mimicking the swings in
intensity that typically occur in competition. However, HIIT protocols can
induce similarly large increases in fitness in recreationally active adults as
well. Although the intensity of the intervals in the Tabata study was
supramaximal, more recent studies have demonstrated that modified versions
of the 20 s on/10 s off protocol can yield similar results with submaximal
intensities that are still very high intensity, ranging from 80% to 95% of O2max.
These aerobic intervals are more appropriate for the general population and
are frequently utilized in group fitness and personal training settings.
Although somewhat counterintuitive because of the high heart rates
achieved, a growing number of fitness experts are suggesting that HIIT should
be considered as a strategy to improve cardiovascular and metabolic health.
Studies of nonathletes training with high-intensity intervals have documented
improved metabolic rate and fat oxidation, decreased abdominal fat, greater
insulin sensitivity, improved blood glucose, and reduced blood pressure after
training. A report from a research team in the United Kingdom showed that
doing 20 s Tabata-style intervals for just 3 min a week improved insulin
sensitivity in young men.3 The authors reasoned that when insulin works more
effectively, the muscles utilize more fatty acid oxidation for fuel, which in turn
may result in greater utilization of fat even at rest. Indeed, the postexercise
oxygen consumption following a 4 min bout of HIIT was double what it was
just before exercise. The extra calories and potential for increased fat
utilization resulting from HIIT may be an untapped resource to safely improve
health outcomes, even in people who are not regularly physically active.
High-Intensity Interval Training (HIIT)
536
Traditionally, exercise physiologists have recommended one of three
regimens to improve aerobic power: continuous exercise at a
moderate to high intensity; long, slow (low-intensity) exercise; or
interval training. However, a growing body of research suggests that
high-intensity interval training (HIIT) is a time-efficient way to
induce many adaptations normally associated with traditional
endurance training. Scientists at McMaster University in Canada have
studied the effects of training using short bursts of very intense
cycling, interspersed with up to a few minutes of rest or low-intensity
cycling for recovery.6 A common training mode employed is based on
the Wingate test, a test that consists of 30 s of all-out cycling and
generally produces mean power outputs that are two to three times
higher than what subjects typically generate during a maximal oxygen
uptake test.
A typical HIIT workout consists of four to six bouts of 30 s all-out
cycling separated by a few minutes of recovery. Therefore, the total
exercise time is as little as 2 min spread over a 20 min total time
period. Several studies have now confirmed that performing six or so
sessions of this type of interval training over a 2-week span can
dramatically improve aerobic capacity in previously untrained
individuals. The best feature of this type of training for busy
exercisers is that such a regimen involves only 15 min total of all-out
cycling within a total time commitment of 2.5 h!5
In addition to improving O2max, HIIT has been proven to have
additional health benefits. Similar to continuous aerobic training
programs, HIIT improves glucose control and insulin sensitivity,
especially in individuals with (or at risk for) type 2 diabetes. HIIT has
also been shown to improve vascular endothelial function, a measure
of blood vessel health. In fact, studies have demonstrated that HIIT
may be more effective than continuous, long-duration training in
promoting metabolic and cardiovascular adaptations.10
HIIT for Athletes
Can highly fit individuals and endurance athletes also benefit from
HIIT? In sedentary individuals, exercise training affects both the
cardiovascular system and the muscles’ oxidative enzyme capacity,
resulting in an increase in O2max. In contrast, in already trained
537
individuals, an increase in exercise intensity close to or even slightly
above O2max is often necessary to elicit improvements in O2max and
performance.
There is growing evidence that inserting HIIT into an already highvolume traditional aerobic training program can further enhance
performance.5 For example, when a group of well-trained cyclists
replaced 15% of their normal training time with HIIT, they improved
their peak power and speed during a 4 km time trial. Such
improvement was seen after only six HIIT sessions inserted over a 4week period.
RESEARCH PERSPECTIVE 9.3
Exploring the Mechanisms That Increase
HIIT
O2max with
High-intensity interval training (HIIT) significantly improves maximal oxygen
uptake ( O2max). In untrained individuals, HIIT can increase O2max to the
same extent as moderate-intensity continuous training, despite the much
shorter duration of exercise bouts. The mechanisms by which moderateintensity aerobic training increases O2max (e.g., greater blood volume, higher
cardiac output, increases in stroke volume) are well characterized and
discussed in detail in this chapter. However, despite the widely seen increases
in O2max in response to HIIT, the specific adaptations that underlie this
538
outcome have not been clarified. According to the Fick equation, increases in
O2max are mediated by increases in cardiac output or arterial–venous oxygen
difference, or (a-v)O2 difference. However, the scientific evidence is not clear
whether HIIT improves one, the other, or both.
Recently, a study conducted by a team of scientists from Cal State San
Marcos, SUNY Stony Brook, and the National College of Natural Medicine
examined the cardiovascular adaptations to 6 weeks of HIIT in 71 healthy,
active, young subjects.2 The aims of this study were (1) how HIIT improves
O2max and (2) whether there is an optimal HIIT regimen that would produce the
most benefit. In order to test this, the subjects were divided into four groups: a
sprint interval-training group (SIT), a high-volume interval-training group
(HIITHI), a periodized interval-training group (PER), and a control group that
did not exercise (CON). For the first 10 exercise sessions, all subjects in the
exercising groups performed the same HIIT protocol of 8 to 10 bouts of 60 s of
cycling at 90% to 110% of peak power with 75 s of recovery between bouts.
After this initial training, the subjects were randomized into their specific
regimens for the remainder of the study. O2max, maximal cardiac output,
stroke volume, heart rate, and the (a-v)O2 difference were measured during
progressive cycling exercise at the beginning of the study, at the midway point,
and at the end of the study. Compared to the control group, all HIIT groups
had a significant increase in O2max, and the magnitude of the increase in
O2max was not different between regimens. In all HIIT groups, maximal cardiac
output and stroke volume increased, while maximal heart rate and the (a-v)O2
difference did not change. Because HIIT increased maximal cardiac output but
did not affect extraction, the study team concluded that HIIT increases O2max
by improving oxygen delivery through increased blood flow rather than by
increasing the muscles’ ability to extract oxygen.
Another study used a type of HIIT training called the 10-20-30
concept (5 min intervals alternating between low speed for 30 s,
moderate speed for 20 s, and close to maximal speed for 10 s) to
assess whether 7 weeks of HIIT training could improve endurance
performance, cardiovascular fitness, and overall physical health in a
group of already well-trained individuals.7 The athletes who
underwent the HIIT training increased their
O2max by 4% and
increased their performance in both 1,500 m and 5 km runs, despite a
~50% reduction in their total training time. They also had a significant
reduction in their total blood cholesterol, cholesterol fractions, and
resting blood pressure. These results suggest that high-intensity
interval training is capable of improving
O2max, exercise
539
performance, and overall markers of cardiovascular health in
previously trained individuals. This same group of researchers had
previously demonstrated an increase in peripheral muscle membrane
proteins and transporters and changes in muscle oxidative enzyme
capacity in previously trained athletes who followed a traditional HIIT
regimen.9
For busy athletes, HIIT training is easily achievable and effective at
improving cardiovascular health as well as athletic performance. It
may be also useful for athletes who wish to reduce their training time
or volume before competition without sacrificing continued
improvements in O2max and performance.
Gibala and Jones recommend that for endurance athletes, 75% of
total training volume be performed at continuous low intensities with
10% to 15% done using high-intensity intervals.5 While each bout of
activity is anaerobic, the overall effect of HIIT is to stimulate
adaptations similar to those with endurance training but in a shorter
period of time and with less total work performed. Studies that have
compared HIIT to a much higher total volume of traditional continuous
endurance training have shown similar improvements in O2max and
cellular markers of improved aerobic capacity in untrained individuals.
Adaptations were different in highly trained athletes. These
adaptations are discussed in more detail in chapter 11.
High-Intensity Interval Training in Team Sports
The science of training athletes depends heavily on the concept of
specificity of training. However, designing a training regimen that
provides sport-specific performance benefits while maintaining overall
speed, fitness, and athletic skills—without overtraining—is often a
difficult task. Adding HIIT to traditional endurance workouts has
gained popularity for its benefits in improving sport-specific athletic
performance,7,9 but most of the studies examining the effects of HIIT
have been performed on athletes competing in individual sports, such
as runners and cyclists, not in athletes who participate in team sports.
In order to determine whether HIIT training would be beneficial for
performance, a group of elite soccer players were tested before, and
again after, a 5-week HIIT intervention. The Danish Second Division
players averaged 2.7 training sessions per week, with each session
540
lasting 3.6 h, and played one match per week. The HIIT,
accomplished by carrying out drills without the ball, consisted of six to
nine 30 s intervals per week at an intensity of 90% to 95% of O2max.
The number of HIIT intervals increased each week. The performance
evaluation included a sprint test, an agility test, and repeated 20 m
shuttle runs at progressively increasing speeds. After the HIIT
intervention, the elite soccer players performed better on the shuttle
runs by 11%, but performance on the sprint and agility tests was
unchanged. Interestingly, after the HIIT interventions, the O2max was
unchanged, but there was a reduction in the athletes’ O2 during
running at a fixed speed of 10 km/h, indicating that running economy
was improved by HIIT in these elite soccer players.
541
In Review
Anaerobic and aerobic power training programs are designed to train the three
metabolic energy systems: the ATP-PCr system, the anaerobic glycolytic system,
and the oxidative system.
Interval training consists of repeated bouts of high- to moderate-intensity exercise
interspersed with periods of rest or reduced-intensity exercise. For short intervals,
the rate or pace of activity and the number of repetitions are usually high, and the
recovery period is usually short. Just the opposite is the case for long intervals.
Both the exercise rate and the recovery rate can be closely monitored with use of
a heart rate monitor.
Interval training is appropriate for all sports. The length and intensity of intervals
can be adjusted based on the sport requirements.
Continuous training has no rest intervals and can vary from LSD training to highintensity training. Long, slow distance training is very popular for general fitness
training.
Fartlek training, or speed play, is an excellent activity for recovering from several
days or more of intense training.
Interval-circuit training combines interval training and circuit training into one
workout.
High-intensity interval training is a time-efficient way to induce many adaptations
normally associated with traditional endurance training. In addition to consuming
less time, it can be used to provide variety to the training.
High-intensity interval training has been shown to improve performance in
already-trained individuals, including those participating in team sports such as
soccer.
542
IN CLOSING
In this chapter, we reviewed general principles of training and the terminology
used to describe these principles. We then learned the essential ingredients of
successful resistance training and anaerobic and aerobic power training
programs. With this background, we can now focus on how the body adapts to
these different types of training programs. In the next chapter, we will see how
the body responds to resistance training.
KEY TERMS
1-repetition maximum (1RM)
aerobic power
anaerobic power
continuous training
eccentric training
electrical stimulation
Fartlek training
free weights
high-intensity interval training (HIIT)
hypertrophy
interval-circuit training
interval training
isokinetic training
isometric training
long, slow distance (LSD) training
muscular endurance
plyometrics
power
principle of individuality
principle of periodization
principle of progressive overload
principle of reversibility
principle of specificity
principle of variation
static-contraction resistance training
strength
variable-resistance training
STUDY QUESTIONS
543
1.
Define and differentiate the terms strength, power, and muscular
endurance. How does each component relate to athletic performance?
2.
Define aerobic and anaerobic power. How does each relate to athletic
performance?
3.
Describe and provide examples for the principles of individuality, specificity,
reversibility, progressive overload, and variation.
4.
What factors need to be considered when one is designing a resistance
training program?
5.
What would be the appropriate range for resistance and repetitions when
one is designing a resistance training program targeted to develop
strength? Muscular endurance? Muscular power? Hypertrophy?
6.
Describe the various types of resistance training, and explain the
advantages and disadvantages of each.
7.
What type of training program would likely provide the greatest
improvement for sprinters? Marathon runners? Football players?
8.
What are some advantages of exercising in a group setting rather than
alone?
9.
Describe the various forms of interval and continuous training programs,
and discuss the advantages and disadvantages of each. Indicate the sport
or event most likely to benefit from each one.
10.
High-intensity interval training has been shown to cause beneficial
adaptations leading to improved performance. Describe those physiological
adaptations.
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
544
545
10
Adaptations to Resistance Training
In this chapter and in the web study guide
Resistance Training and Gains in Muscular Fitness
ACTIVITY 10.1 What Causes Strength Gains? explores the roles of neural adaptations and
hypertrophy in strength gains.
Mechanisms of Gains in Muscle Strength
Neural Control of Strength Gains
Muscle Hypertrophy
Integration of Neural Activation and Fiber Hypertrophy
Muscle Atrophy and Decreased Strength with Inactivity
Fiber Type Alterations
ANIMATION FOR FIGURE 10.4 breaks down the satellite cell response to muscle injury.
Interaction Between Resistance Training and Diet
Recommendations for Protein Intake
Mechanism of Protein Synthesis with Resistance Training and Protein Intake
VIDEO 10.1 presents Luc von Loon on the role of protein in adaptations to resistance training.
ANIMATION FOR FIGURE 10.7 shows the effects of resistance training, insulin, and amino acid intake
on skeletal muscle protein synthesis.
ACTIVITY 10.2 The Building Blocks for Increased Strength and Mass reviews a variety of factors
involved in muscle hypertrophy and how these factors interact, which can be a helpful part of
developing effective training programs.
Resistance Training for Special Populations
Resistance Exercise for Older Adults
Resistance Training for Children
Resistance Training for Athletes
In Closing
546
W
hen he died on September 13, 2013, at the age of 84, few sport fans
had heard of Jim Bradford. Bradford, an African American, spent much of his life
working quietly behind the scenes at the Library of Congress as a researcher and
bookbinder. At the 1952 Olympic Games in Helsinki and again at the 1960 Games
in Rome, Bradford won silver medals in the weightlifting heavyweight division. Yet
he was hardly known in his hometown of Washington in those decades, let alone
nationally. Although it’s hard to imagine in today’s world of professional athletes,
Bradford had to take unpaid leave from the Library of Congress to compete in the
Olympics. “I come back to my job and that is it. That was par for the course then.”2
Mr. Bradford was a self-proclaimed “butterball” during high school who started
lifting weights after reading inspirational stories in a weightlifting magazine. He
started with a set of dumbbells in his second-floor bedroom before moving his
training to a nearby YMCA at his parents’ request. There, he developed a unique
lifting style—keeping his legs together and bending his back only as he lifted the
bar overhead—for the simple reason that he feared dropping the weights, scuffing
the floor, and getting kicked out of the gym!2
With any type of effective chronic exercise, multiple adaptations
occur in the neuromuscular system. The type and extent of the
adaptations depend on the type of training: Aerobic training, such as
running, cycling, or swimming, results in little gain in muscle size and
strength, but major neuromuscular adaptations occur with
resistance training.
Resistance training was once considered inappropriate for
athletes except those in competitive weightlifting, throwing events in
track and field, and wrestling and boxing. Women typically avoided
the weight room for fear of becoming masculine looking! But in the
late 1960s and early 1970s, coaches and researchers discovered
that strength and power training are beneficial for almost all sports
and activities, and for women as well as men. It was not until the late
1980s and early 1990s that health professionals began to recognize
the importance of resistance training to overall health, fitness, and
rehabilitation.
Most athletes now include resistance training as an important
component of their overall training program. Much of this attitude
547
change is attributable to research that has proven the performance
benefits of resistance training and to innovations in training
techniques and equipment. Resistance training is now an important
part of the exercise prescription for all those who seek the healthrelated benefits of exercise.
Resistance Training and Gains in Muscular
Fitness
Throughout this book, we see how important muscular fitness is to
health, quality of life, and athletic performance. How do we get
stronger and how do we increase muscle power and muscle
endurance? Maintaining an active lifestyle is important in maintaining
muscular fitness, but resistance training is necessary to increase
muscular strength and power. In this section, we briefly review the
changes that result from resistance training. We focus on strength,
with only a brief mention of power and muscular endurance—topics
that are discussed in more detail later in this book.
The neuromuscular system is one of the most responsive systems
in the body to the repeated stimulation of training. Resistance
training programs can produce substantial strength gains. In 3 to 6
months, one can see from 25% to 100% improvement, sometimes
even more. These estimates of percentage gains in strength are,
however, somewhat misleading. Most subjects in strength training
research studies have never lifted weights or participated in any
other form of resistance training. Most of their early gains in strength
are the result of learning how to more effectively produce force and
produce a true maximal movement, such as moving a barbell from
the chest to a fully extended position in the bench press. This
learning effect can account for as much as 50% of the early strength
gains.
Muscle is very plastic, increasing in size and strength with training
and decreasing in size and strength when immobilized. The
remainder of this chapter details the physiological adaptations that
allow people to become stronger.
Mechanisms of Gains in Muscle Strength
548
For many years, strength gains were assumed to result directly from
increases in muscle size (hypertrophy). This assumption was logical
because many people who regularly strength trained developed
visually larger muscles. Also, muscles associated with a limb
immobilized in a cast for weeks or months start to decrease in size
(atrophy) and lose strength almost immediately. Gains in muscle
size are generally paralleled by gains in strength, and losses in
muscle size correlate highly with losses in strength. Thus, it is
tempting to conclude that a direct cause-and-effect relationship
exists between muscle size and muscle strength. While there is an
association between size and strength, muscle strength involves far
more than mere muscle size.
This does not mean that muscle size is unimportant in the ultimate
strength potential of the muscle. The ability to generate force
depends on the number of cross-bridges within sarcomeres, which in
turn depends on the amount of actin and myosin. Size is extremely
important, as revealed by the existing men’s and women’s world
records for competitive weightlifting, shown in figure 10.1. As weight
classification increases (implying increased muscle mass), so does
the record for the total weight lifted. However, the mechanisms
associated with strength gains are more complex. What, in addition
to increased size of the muscle, explains strength gains with
training? Let’s first consider the strong evidence that neural control
of the muscle is altered with resistance training, allowing for a
greater force production.
RESEARCH PERSPECTIVE 10.1
Aerobic Benefits From Resistance Exercise Training
Resistance exercise training is a well-established method for increasing
muscle size and strength. The classical skeletal muscle responses to
resistance exercise training (e.g., hypertrophy, changes in muscle fiber type,
increases in neural activation) are described in detail in this chapter.
However, the long-held dogma that resistance exercise training results in
distinctly different adaptations from aerobic exercise training (which are
discussed in detail in chapter 11) has limited many studies to a strict focus on
the mechanisms of muscle hypertrophy and gains in strength.
Conversely, increases in skeletal muscle mitochondrial number and
function and increases in the number and density of capillaries in the skeletal
549
muscle are both well-known adaptations to aerobic exercise training. These
adaptations increase ATP production and oxygen and nutrient delivery to the
exercising skeletal muscle; as such, they contribute to the improvements in
muscle health and maximal oxygen uptake that occur with aerobic exercise
training. In addition to improving fitness, increases in mitochondrial function
and skeletal muscle capillarization also enhance overall health by improving
muscle bioenergetics, insulin sensitivity, and glucose tolerance at rest.
Therefore, strategies to induce these adaptations may have benefits for many
people, not just athletes.
Recently, exercise physiologists have begun to explore whether
resistance exercise training may also exert some of these aerobic benefits.
Research studies conducted at the University of Texas Medical Branch17 and
Maastricht University in the Netherlands26 are two of the first to explore this
possibility. Both of these studies utilized a 12-week program of resistance
exercise training to improve muscular fitness and collected muscle biopsy
samples from the vastus lateralis before and after the training program (see
figure). In Texas, the research team compared mitochondrial respiratory
capacity, measured as citrate synthase activity, in the muscle biopsy samples
from young subjects. They found that resistance exercise increased
mitochondrial protein expression and respiratory capacity, suggesting that
this resistance training protocol improved the oxidative capacity of the trained
muscle. The Netherlands group examined the number of capillary contacts
and the ratio of capillaries to muscle fibers in muscle biopsy samples from
young and older men at baseline, and in the older men again after the
resistance training protocol. (They chose to study resistance training in the
older men only, opining that these subjects might have the most clinical
benefit from resistance exercise to fight sarcopenia.) They found that older
men had fewer capillary contacts and a lower ratio of capillaries to muscle
fibers compared to young men, but, importantly, both of these aerobic-type
variables increased in the older men after 12 weeks of resistance training.
This led the researchers to conclude that resistance exercise can increase
skeletal muscle capillarization.
Taken together, these studies show that the adaptations to resistance
exercise may have more in common with aerobic exercise adaptations than
we previously thought. Resistance exercise training improves mitochondrial
function and capillarization in the skeletal muscle. These findings increase
our understanding of how resistance exercise improves multiple fitness
domains and gives us new knowledge about the health benefits of resistance
training.
550
Twelve weeks of resistance training increases mitochondrial respiration17 and the
number of capillary contacts per muscle fiber26 in trained skeletal muscle. These
adaptations were previously thought to occur with aerobic exercise training only.
However, resistance exercise training can induce these aerobic adaptations in the
trained muscle as well.
Neural Control of Strength Gains
An important component of the strength gains that result from
resistance training, especially in the early stages, are neural
adaptations. Enoka has made a convincing argument that strength
gains can be achieved without structural changes in muscle but not
without neural adaptations.7 Thus, strength is not solely a property of
muscle but rather a property of the neuromotor system. Motor unit
recruitment, frequency of motor nerve firing rates, better
synchronization of motor units during a particular movement, and
other neural factors are important to strength gains. Removal of
neural inhibition may also play a role. These neural factors may well
explain most, if not all, strength gains that occur in the absence of
hypertrophy, as well as episodic superhuman feats of strength.
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FIGURE 10.1 World records for (a) the snatch, (b) the clean and jerk, and (c) total weight for men
and women through 2016.
Synchronization and Recruitment of Additional Motor Units
Motor units are generally recruited asynchronously; they are not all
engaged at the same instant. They are controlled by a number of
different neurons that can transmit either excitatory or inhibitory
impulses (see chapter 3). Whether the muscle fibers contract or stay
relaxed depends on the summation of the many impulses received
by the given motor unit at any one time. The motor unit is activated
and its muscle fibers contract only when the incoming excitatory
impulses exceed the inhibitory impulses and the threshold is met or
exceeded.
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Strength gains may result from changes in the connections
between motor neurons located in the spinal cord, allowing motor
units to act more synchronously. This increased synchronicity means
that a greater number of motor units will be firing at any one time,
facilitating contraction and increasing the muscle’s ability to generate
force. There is good evidence to support increased motor unit
synchronization with resistance training, but controversy still exists
as to whether synchronization of motor unit activation produces a
more forceful contraction. It is clear, however, that synchronization
does improve the rate of force development and the capability to
exert steady forces.6
Increased Rate Coding of Motor Units
The increase in neural drive of α-motor neurons could also increase
the frequency of discharge, or rate coding, of their motor units.
Recall from chapter 1 that as the frequency of stimulation of a given
motor unit increases, the muscle eventually reaches a state of
tetanus, producing the absolute peak force or tension of the muscle
fiber or motor unit (see figure 1.14). There is limited evidence that
rate coding is increased with resistance training. Rapid movement or
ballistic-type training appears to be particularly effective in
stimulating increases in rate coding.
Increased Neural Drive
Neural drive refers to the combination of motor unit recruitment and
rate coding of the units. Neural drive starts in the central nervous
system and is spread to muscle fibers through peripheral nerves.
Electromyography (EMG) using surface electrodes over the muscle
measures the total activity within the nerve and muscle and therefore
is a good measure of neural drive.
An alternate explanation for neutrally mediated strength gains is
simply that more motor units are recruited to perform the given task,
independent of whether these motor units act in unison. Such
improvement in recruitment patterns could result from an increase in
neural drive to the α-motor neurons during maximal contraction.
Trained muscles generate a given amount of submaximal force with
less EMG activity, suggesting a more efficient motor unit recruitment
pattern. This increase in neural drive could increase the frequency of
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discharge (rate coding) of the motor units or reduce inhibitory
impulses, allowing more motor units to be activated or to be
activated at a higher frequency. Additionally, maximal neural drive
appears to increase with resistance training.
Autogenic Inhibition
Inhibitory mechanisms in the neuromuscular system, such as the
Golgi tendon organs, might be necessary to prevent the muscles
from exerting more force than the bones and connective tissues can
tolerate. This control is referred to as autogenic inhibition.
However, under extreme situations when larger forces are
sometimes produced, significant damage can occur to these
structures, suggesting that the protective inhibitory mechanisms can
be overridden.
The function of Golgi tendon organs is discussed in chapter 3.
When the tension on a muscle’s tendons and internal connective
tissue structures exceeds the threshold of the embedded Golgi
tendon organs, motor neurons to that muscle are inhibited; that is,
autogenic inhibition occurs. Both the reticular formation in the brain
stem and the cerebral cortex function to initiate and propagate
inhibitory impulses.
Resistance training can gradually reduce or counteract these
inhibitory impulses, allowing the muscle to achieve a greater force
production independent of increases in muscle mass. Thus, strength
gains may be achieved by reduced neurological inhibition. This
theory is attractive because it can at least partially explain
superhuman feats of strength and strength gains in the absence of
hypertrophy.
Other Neural Factors
In addition to increasing motor unit recruitment or decreasing
neurological inhibition, other neural factors can contribute to strength
gains with resistance training. One of these is referred to as
coactivation of agonist and antagonist muscles (the agonist muscles
are the primary movers, and the antagonist muscles act to impede
the agonists). If we use forearm flexor concentric contraction as an
example, the biceps is the primary agonist and the triceps is the
antagonist. If the two were contracting with equal force development,
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no movement would occur. Thus, to maximize the force generated
by an agonist, it is necessary to minimize the amount of coactivation.
Reduction in coactivation could explain a portion of strength gains
attributed to neural factors, but its contribution likely would be small.
Changes also have been noted in the morphology of the
neuromuscular junction, with both increased and decreased activity
levels that might be directly related to the muscle’s force-producing
capacity.
Muscle Hypertrophy
How does a muscle’s size increase? Two types of hypertrophy can
occur: transient and chronic. Transient hypertrophy is the
increased muscle size that develops during and immediately
following a single exercise bout. This results mainly from fluid
accumulation (edema) in the interstitial and intracellular spaces of
the muscle that comes from the blood plasma. Transient
hypertrophy, as its name implies, lasts only for a short time. The fluid
returns to the blood within hours after exercise.
Chronic hypertrophy refers to the increase in muscle size that
occurs with long-term resistance training. This reflects actual
structural changes in the muscle that can result from an increase in
the size of existing individual muscle fibers (fiber hypertrophy), in
the number of muscle fibers (fiber hyperplasia), or in both.
Controversy surrounds the theories that attempt to explain the
underlying cause of this phenomenon. Of importance, however, is
the finding that the eccentric component of training is important in
maximizing increases in muscle fiber cross-sectional area. A number
of studies have shown greater hypertrophy and strength resulting
solely from eccentric contraction training as compared to concentric
contraction or combined eccentric and concentric contraction
training. Further, higher-velocity eccentric training appears to result
in greater hypertrophy and strength gains than slower-velocity
training.20 These greater increases appear to be related to
disruptions in the sarcomere Z-lines. This disruption was originally
labeled muscle damage but is now thought to represent fiber protein
remodeling.20 Thus, training with only concentric actions could limit
muscle hypertrophy and increases in muscle strength.
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Intensity and Hypertrophy
With traditional training methods, the prevailing opinion has been
that an intensity of 60% to 85% of 1RM or higher is needed to
achieve substantial increases in muscle size.
More recently, however, research has suggested that low-intensity
exercise at <50% of 1RM can lead to gains in muscle size equal to
those seen at high intensities, provided that the training is performed
to volitional muscle fatigue.18 This theory holds that fatiguing
contractions at light loads lead to metabolic stimuli that result in
maximal muscle fiber recruitment.
Is there a minimal intensity for resistance training that will lead to
muscle hypertrophy, provided that resistance exercises are
performed to volitional fatigue? It has been reported that from
intensities as low as 30% and as high as 90% of 1RM, load played a
minimal role in stimulating muscle protein synthesis, muscle
hypertrophy, and strength gains in novice exercisers.3 High-repetition
(HR) and low-repetition (LR)—low and high load, respectively—
training caused similar increases in skeletal muscle mass when
resistance exercise was performed until volitional failure. Increases
in lean body mass, as an indirect measure of muscle mass, and
muscle fiber CSA, a direct measure of muscle area, occurred in both
LR and HR groups with no differences between groups. There was a
significant increase in 1RM strength for the leg press, knee
extension, and shoulder press exercises, again with no differences
between groups. These effects do not seem to depend on training
status because similar results occurred in men with previous
strength-training experience.16
The following section examines the two postulated mechanisms
for increasing muscle size with resistance training: fiber hypertrophy
and fiber hyperplasia.
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Fiber Hypertrophy
Early research suggested that the number of muscle fibers in each of
a person’s muscles was established by birth or shortly thereafter and
that this number remained fixed throughout life. If this were true, then
whole-muscle hypertrophy could result only from individual muscle
fiber hypertrophy. This could be explained by
more myofibrils,
more actin and myosin filaments,
more sarcoplasm,
more connective tissue, or
any combination of these.
As seen in the micrographs in figure 10.2, effective resistance
training can significantly increase the cross-sectional area of muscle
fibers. Such dramatic enlargement of muscle fibers does not occur,
however, in all cases of muscle hypertrophy.
Muscle fiber hypertrophy is probably caused by increased
numbers of myofibrils and actin and myosin filaments, which would
provide more cross-bridges for force production during maximal
contraction. The size of existing myofibrils does not appear to
change. The increase in muscle cross-sectional area results from
adding new sarcomeres in parallel to each other.
Individual muscle fiber hypertrophy from resistance training
appears to result from a net increase in muscle protein synthesis.
The muscle’s protein content is in a continual state of flux. Protein is
always being synthesized and degraded. But the rates of these
processes vary with the demands placed on the body. During
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exercise, protein synthesis decreases, while protein degradation
increases. After exercise, although protein degradation continues,
protein synthesis increases three- to fivefold more, leading to a net
synthesis of myofibrillar (myosin and actin) protein. A single bout of
resistance exercise can elevate net protein synthesis for up to 24 h.
Hormones and Hypertrophy
The prevailing perspective in muscle physiology is that the hormone
changes induced by resistance exercise facilitate increases in
muscle mass that in turn increase muscular strength. The hormones
that are typically associated with this response include the anabolic
hormones testosterone, growth hormone (GH), and insulin-like
growth factor 1 (IGF-1). The hormone testosterone has traditionally
been thought to be at least partly responsible for these changes
because one of its primary functions is promoting muscle growth.
Testosterone is a steroidal hormone with major anabolic functions,
and men experience a significantly greater increase in muscle
growth starting at puberty, which is largely due to a 10-fold increase
in testosterone production. Furthermore, it has been well established
that massive doses of anabolic steroids coupled with resistance
training markedly increase muscle mass and strength (see chapter
16).
FIGURE 10.2 Microscopic views of muscle cross sections taken from the leg muscle of a man who
had not trained during the previous 2 years, (a) before he resumed training and (b) after he completed
6 months of dynamic strength training. Note the significantly larger fibers (hypertrophy) after training.
While it is true that acute resistance training transiently increases
the concentrations of these hormones, it has been shown
experimentally that acute increases in these hormones are not
required for increases in muscle mass or strength.19 Researchers at
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McMaster University designed a series of studies to examine
whether exercise-induced elevations in testosterone, GH, and IGF-1
were necessary for, or could enhance, muscle anabolism. They
examined the elbow flexor muscles when exposed (1) to low
hormone concentrations during a small muscle mass exercise
consisting of isolated arm curls and (2) to high circulating hormone
concentrations induced by an intense lower body exercise routine in
addition to arm curls.29,30,31 In the low hormone trials, myofibrillar
protein synthesis was elevated after acute exercise bouts, and there
were gains in strength and hypertrophy after training—even though
testosterone, GH, and IGF-1 all remained near baseline
concentrations. This implies that postexercise increases in these
hormones are not necessary to stimulate muscle anabolism.
Furthermore, when these hormones were elevated postexercise,
there was no further enhancement in myofibrillar protein synthesis or
gain in strength and hypertrophy with training.
In addition to these studies, researchers have compared men’s
and women’s responses to resistance training. Women have a 45fold lower postexercise testosterone response compared to men
even after their 20-fold lower baseline testosterone concentration is
accounted for.28 Despite having drastically lower postexercise
increases in testosterone, the women were able to robustly increase
rates of myofibrillar protein synthesis. Moreover, as in most exercise
training studies, the men and women trained in this study had
variable individual responses in terms of muscle hypertrophy.
Despite these variable responses, there was no relation between
each subject’s exercise-induced increases in testosterone, GH, and
IGF-1 and his or her muscle growth or strength gains.32
These new data provide strong new evidence that postexercise
elevations in testosterone, GH, and IGF-1 are not required to
increase muscle anabolism and strength. An alternate hypothesis is
that the muscle hypertrophy and strength gains occurring with
resistance training are mediated by changes in intrinsic
intramuscular properties.
Fiber Hyperplasia
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Research on animals suggests that hyperplasia, an increase in the
total number of fibers within a muscle, may also be a factor in the
hypertrophy of whole muscles. Studies on cats provide fairly clear
evidence that fiber splitting occurs with extremely heavy weight
training.8 Cats were trained to move a heavy weight with a forepaw
to get their food (figure 10.3). With the use of food as a powerful
incentive, they learned to generate considerable force. With this
intense strength training, selected muscle fibers appeared to actually
split in half, and each half then increased to the size of the parent
fiber.
FIGURE 10.3 Heavy resistance training in cats.
Subsequent studies, however, demonstrated that hypertrophy of
selected muscles in chickens, rats, and mice resulting from chronic
exercise overload was attributable solely to hypertrophy of existing
fibers, not hyperplasia. In these studies, each fiber in the whole
muscle was actually counted. These direct fiber counts revealed no
change in fiber number.
This finding led the scientists who performed the initial cat
experiments to conduct an additional resistance training study with
cats. This time they used actual fiber counts to determine if total
muscle hypertrophy resulted from hyperplasia or fiber hypertrophy.9
Following a resistance training program of 101 weeks, the cats were
able to perform one-leg lifts of an average of 57% of their body
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weight, resulting in an 11% increase in muscle weight. Most
important, the researchers found a 9% increase in the total number
of muscle fibers, confirming that muscle fiber hyperplasia did occur.
The difference in results between the cat studies and those with
rats and mice most likely is attributable to differences in the manner
in which the animals were trained. The cats were trained with a pure
form of resistance training: high resistance and low repetitions. The
other animals were trained with more endurance-type activity: low
resistance and high repetitions.
One additional animal model has been used to stimulate muscle
hypertrophy associated with hyperplasia. Scientists have placed the
anterior latissimus dorsi muscle of chickens in a state of chronic
stretch by attaching weights to it, with the other wing serving as the
normal control condition. In many of the studies that have used this
model, the chronic stretch has resulted in substantial hypertrophy
and hyperplasia.
Researchers are still uncertain about the roles played by
hyperplasia and individual fiber hypertrophy in increasing human
muscle size with resistance training. Most evidence indicates that
individual fiber hypertrophy accounts for most whole-muscle
hypertrophy. However, results from selected studies indicate that
hyperplasia is possible in humans. It is possible that only very high
intensity in resistance training can result in fiber hyperplasia, and
even then, the percentage of the total muscle size increase due to
this phenomenon is small, perhaps 5% to 10%. Whether strength
training results in muscle fiber hyperplasia in humans remains
unresolved.
In a cadaver study of seven previously healthy young men who
had suffered sudden accidental death, the investigators compared
cross sections of autopsied right and left tibialis anterior muscles
(lower leg). Right-hand dominance is known to lead to greater
hypertrophy of the left leg. In fact, the average cross-sectional area
of the left muscle was 7.5% larger than that of the right. This was
associated with a 10% greater number of fibers in the left muscle.
There was no difference in mean fiber size.21
The differences between these studies might be explained by the
nature of the training load or stimulus. Training at high intensities or
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high resistances is thought to cause greater fiber hypertrophy,
particularly of the type II (fast-twitch) fibers, than training at lower
intensities or resistances.
Only one longitudinal study demonstrated the possibility of
hyperplasia in men who had previous recreational resistance training
experience.14 Following 12 weeks of intensified resistance training,
the muscle fiber number in the biceps brachii of several of the 12
subjects appeared to increase significantly. It appears from this study
that hyperplasia can occur in humans but possibly only in certain
subjects or under certain training conditions.
From the preceding information, it appears that fiber hyperplasia
can occur in animals and possibly in humans. How are these new
cells formed? It is postulated that individual muscle fibers have the
capacity to divide and split into two daughter cells, each of which can
then develop into a functional muscle fiber. Importantly, satellite
cells, which are the myogenic stem cells involved in skeletal muscle
regeneration, are likely involved in the generation of new muscle
fibers. These cells are typically activated by muscle stretching and
injury; as we see later in this chapter, muscle injury results from
intense training, particularly eccentric-action training. Muscle injury
can lead to a cascade of responses in which satellite cells become
activated and proliferate, migrate to the damaged region, and fuse to
existing myofibers or combine and fuse to produce new myofibers.13
This is illustrated in figure 10.4.
Satellite cells provide additional nuclei within muscle fibers. The
added genetic machinery (DNA) is necessary to provide the
increased muscle protein content and related materials to facilitate
hypertrophy (and theoretically, hyperplasia).
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FIGURE 10.4 The satellite cell response to muscle injury.
Adapted by permission from T.J. Hawke and D.J. Garry, “Myogenic Satellite Cells: Physiology to Molecular
Biology,” Journal of Applied Physiology 91 (2001): 534-551.
Integration of Neural Activation and Fiber Hypertrophy
Research on resistance training adaptations indicates that early
increases in voluntary strength, or maximal force production, are
associated primarily with neural adaptations resulting in increased
voluntary activation of muscle. This was clearly demonstrated in a
study of both men and women who participated in an 8-week, highintensity resistance training program, training twice per week.22
Muscle biopsies were obtained at the beginning of the study and
every 2 weeks during the training period. Strength, measured
according to the 1RM, increased substantially over the 8 weeks of
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training, with the greatest gains coming after the second week.
Muscle biopsies, however, revealed only a small, insignificant
increase in muscle fiber cross-sectional area by the end of the 8
weeks of training. Thus, the strength gains were largely the result of
increased neural activation.
Long-term increases in strength generally result from hypertrophy
of the trained muscle. However, because it takes time to build protein
through a decrease in protein degradation, an increase in protein
synthesis, or both, early strength gains are typically due to changes
in the pattern by which nerves activate the muscle fibers. Most
research shows that neural factors contribute prominently to strength
gains during the first 8 to 10 weeks of training. Hypertrophy
contributes little during these initial weeks of training but
progressively increases its contribution, becoming the major
contributor after 10 weeks of training. However, not all studies
concur with this pattern of strength development. One 6-month study
of strength-trained athletes showed that neural activation explained
most of the strength gains during the most intensive training months
and that hypertrophy was not a major factor.12
Muscle Atrophy and Decreased Strength with Inactivity
When a normally active or highly trained person reduces his or her
level of activity or ceases training altogether, changes occur in both
muscle structure and function. This is illustrated by the results of two
types of studies: studies in which entire limbs have been immobilized
and studies in which highly trained people stop training—so-called
detraining.
Immobilization
When a trained muscle suddenly becomes inactive through
immobilization, major changes are initiated within that muscle in a
matter of hours. During the first 6 h of immobilization, the rate of
protein synthesis starts to decrease. This decrease likely initiates
muscular atrophy, which is the wasting away or decrease in the size
of muscle tissue. Atrophy results from lack of muscle use and the
consequent loss of muscle protein that accompanies the inactivity.
Strength decreases are most dramatic during the first week of
immobilization, averaging 3% to 4% per day. This is associated not
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only with the atrophy but also with decreased neuromuscular activity
of the immobilized muscle.
Immobilization appears to affect both type I and type II fibers.
From various studies, researchers have observed disintegrated
myofibrils, streaming Z-disks (discontinuity of Z-disks and fusion of
the myofibrils), and mitochondrial damage. When muscle atrophies,
the cross-sectional fiber area decreases. Several studies have
shown the effect to be greater in type I fibers, including a decrease in
the percentage of type I fibers, thereby increasing the relative
percentage of type II fibers.
Muscles can and often do recover from immobilization when
activity is resumed. The recovery period is substantially longer than
the period of immobilization.
Cessation of Training
Similarly, significant muscle alterations can occur when people stop
training. In one study, women resistance trained for 20 weeks and
then stopped training for 30 to 32 weeks. The training program
focused on the lower extremity, using a full squat, leg press, and leg
extension. Finally, the participants retrained for 6 weeks.23 Strength
increases were dramatic, as seen in figure 10.5. Compare the
women’s strength after their initial training period (post-20) with their
strength after detraining (pre-6). This represents the strength loss
they experienced with cessation of training. During the two training
periods, increases in strength were accompanied by increases in the
cross-sectional23 area of all fiber types and a decrease in the
percentage of type IIx fibers. Detraining had relatively little effect on
fiber cross-sectional area, although the type II fiber areas tended to
decrease (figure 10.6).
To prevent losses in the strength gained through resistance
training, basic maintenance programs must be established once the
desired goals for strength development have been achieved.
Maintenance programs are designed to provide sufficient stress to
the muscles to maintain existing levels of strength while allowing a
reduction in intensity, duration, or frequency of training.
In one study, men and women resistance trained with knee
extensions for either 10 or 18 weeks and then spent an additional 12
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weeks with either no training or reduced training.10 Knee extension
strength increased 21.4% during the training period. Subjects who
then stopped training lost 68% of their strength gains during the
weeks they didn’t train. But subjects who reduced their training (from
3 days per week to 2, or from 2 to 1) did not lose strength. Thus, it
appears that strength can be maintained for at least up to 12 weeks
with reduced training frequency.
FIGURE 10.5 Changes in muscle strength for 3 different resistance exercises, (a) squat, (b) leg
press, and (c) leg extension, with resistance training in women. Pre-20 values indicate strength before
starting training, post-20 values indicate the changes following 20 weeks of training, pre-6 values
indicate the changes following 30 to 32 weeks of detraining, and post-6 values indicate the changes
following 6 weeks of retraining.
Adapted by permission from R.S. Staron et al., “Strength and Skeletal Muscle Adaptations in Heavy-ResistanceTrained Women After Detraining and Retraining,” Journal of Applied Physiology 70 (1991): 631-640.
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FIGURE 10.6 Changes in mean cross-sectional areas for the major fiber types with resistance training
in women over periods of training (post-20), detraining (pre-6), and retraining (post-6). Type IIa/IIx is an
intermediate fiber type. See figure 10.5 caption for more details.
Fiber Type Alterations
Can muscle fibers change from one type to another through
resistance training? The earliest research concluded that neither
speed (anaerobic) nor endurance (aerobic) training could alter the
basic fiber type, specifically from type I to type II or from type II to
type I. These early studies did show, however, that fibers began to
take on certain characteristics of the opposite fiber type if the training
was of the opposite kind (e.g., type II fibers might become more
oxidative with aerobic training).
Research using animal models has shown that fiber type
conversion is indeed possible under conditions of cross-innervation,
in which a type II motor unit is experimentally innervated by a type I
motor neuron or a type I motor unit is experimentally innervated by a
type II motor neuron. Also, chronic, low-frequency nerve stimulation
transforms type II motor units into type I motor units within a matter
of weeks. Muscle fiber types in rats have changed in response to 15
weeks of high-intensity treadmill training, resulting in an increase in
type I and type IIa fibers and a decrease in type IIx fibers.11 The
transition of fibers from type IIx to type IIa and from type IIa to type I
was confirmed by several different histochemical techniques.
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Staron and coworkers found evidence of fiber type transformation
in women as a result of heavy resistance training.24 Substantial
increases in static strength and in the cross-sectional area of all fiber
types were noted following a 20-week heavy resistance training
program for the lower extremity. The mean percentage of type IIx
fibers decreased significantly, but the mean percentage of type IIa
fibers increased. The transition of type IIx fibers to type IIa fibers with
resistance training has been consistently reported in a number of
subsequent studies. Further, other studies demonstrate that a
combination of high-intensity resistance training and short-interval
speed work can lead to a conversion of type I to type IIa fibers.
In Review
Neural adaptations always accompany the strength gains that result from
resistance training, but hypertrophy may or may not take place.
Neural mechanisms leading to strength gains can include an increase in
frequency of stimulation, or rate coding; recruitment of more motor units; more
synchronous recruitment of motor units; and decreases in autogenic inhibition
from the Golgi tendon organs.
Early gains in strength appear to result more from changes in neural factors, but
later long-term gains are largely the result of muscle hypertrophy.
Transient muscle hypertrophy is the temporary enlargement of muscle resulting
from edema immediately after an exercise bout.
Chronic muscle hypertrophy occurs from repeated resistance training and
reflects actual structural changes in the muscle.
Most muscle hypertrophy results from an increase in the size of individual muscle
fibers (fiber hypertrophy).
Fiber hypertrophy increases the numbers of myofibrils and actin and myosin
filaments, which provides more cross-bridges for force production.
Muscle fiber hyperplasia has been clearly shown to occur in animal models with
the use of resistance training to induce muscle hypertrophy. Only a few studies
suggest evidence of hyperplasia in humans.
Muscles atrophy (decrease in size and strength) when they become inactive, as
with injury, immobilization, or cessation of training.
Atrophy begins very quickly if training is stopped, but training can be reduced, as
in a maintenance program, without resulting in atrophy or loss of strength.
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With resistance training there is a transition of type IIx to type IIa fibers.
Evidence indicates that one fiber type can actually be converted to the other type
(e.g., type I to type II, or vice versa) as a result of cross-innervation or chronic
stimulation, and possibly with training.
Interaction Between Resistance Training and
Diet
Muscle hypertrophy in response to resistance training can be either
limited or enhanced by nutrition. As mentioned previously, a net
positive protein balance (more synthesis than breakdown) is the
necessary condition under which muscle hypertrophy occurs.
Without adequate protein in the diet, protein synthesis is
compromised and muscles cannot increase their protein content and
hypertrophy. Ingesting protein within a few hours after a bout of
resistance exercise increases the rate of protein synthesis and thus
adds to the net positive protein balance. Increased protein intake
over the subsequent 24 h period will continue to support muscle
anabolism. Therefore, nutrition and exercise are powerful stimulators
of skeletal muscle protein synthesis.5
VIDEO 10.1 Presents Luc von Loon on the role of protein in
adaptations to resistance training.
Recommendations for Protein Intake
An international group of researchers recently performed a
systematic analysis of 49 published studies (1,863 subjects) to
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determine if dietary protein supplementation enhances the gains in
muscle mass and strength with resistance training.15 They surveyed
randomized controlled trials in which subjects performed resistance
training for at least 6 weeks and took various amounts of dietary
protein supplementation. Their analysis of this large sample showed
that dietary protein supplementation significantly enhanced changes
in strength as measured by 1-repetition maximum tests and muscle
size (fiber cross-sectional area and whole-muscle cross-sectional
area). However, protein intakes greater than ~1.6 g/kg of body
weight per day did not further contribute to these gains. So, although
the current U.S. Dietary Reference Intake (DRI) for protein for people
over 18 years of age, regardless of physical activity status, is 0.8
g/kg per day, athletes engaged in resistance training may require
protein intakes in the diet as high as 1.7 g/kg per day. Although
ingestion of relatively small amounts of protein (5-10 g) can stimulate
muscle protein synthesis in young men and women, to make
muscles larger, one should consume larger amounts of protein, on
the order of 20 to 25 g, immediately after resistance exercise.1
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What type of protein should be ingested and how much? The best
forms of protein for muscle hypertrophy are easily and rapidly
digested and rich in essential amino acids, especially leucine. Whey
protein found in milk is one source that meets both of these goals. In
practice, after resistance training, athletes should consume a small
amount of high-quality protein along with adequate carbohydrate in
order to stimulate muscle proteins and replenish muscle glycogen
stores after exercise. This can be accomplished with either a
recovery beverage or foods such as milk or yogurt, a small
sandwich, or a protein-rich energy bar. Adding carbohydrate to
postexercise protein ingestion does not markedly affect muscle
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protein balance but does have other benefits, including aiding in the
resynthesis of muscle glycogen.
Is there an optimal timing of protein ingestion when an individual
is trying to optimize the hypertrophic response to successive
exercise sessions? A single bout of exercise stimulates muscle
protein synthesis rates for several hours, and intake of protein further
enhances postexercise muscle protein synthesis. The protein
synthesis–stimulating effect of a single dose of amino acids is
transient and lasts only 1 to 2 h. Ingesting repeated small doses of
protein during recovery from resistance training may be more
effective in increasing muscle hypertrophy than eating just one large
meal. However, elevated muscle protein synthesis rates are not
totally limited to the few hours of acute postexercise recovery. The
so-called window of opportunity lasts from just before the start of
resistance exercise to several hours postexercise. Providing protein
before or during exercise can enhance muscle protein synthesis
during exercise and is a good strategy for prolonged or repeated
workouts.
Mechanism of Protein Synthesis with Resistance Training and
Protein Intake
The rate of protein synthesis within the myofibrils is controlled
primarily by an enzyme, or kinase, known as mTOR (mechanistic
target of rapamycin). mTOR integrates the input from upstream
pathways, including insulin and growth factors and amino acids
(figure 10.7), and controls transcription of messenger RNA (mRNA).
If mTOR is blocked experimentally, resistance exercise does not
result in muscle hypertrophy. The primary stimulus for protein
synthesis is the mechanical stretch applied to the muscle, which
activates mTOR. mTOR senses cellular nutrient and oxygen levels,
so it is also activated by the proper timing of protein intake,
specifically proteins rich in leucine. So, delivering leucine to muscles
during the window of opportunity will increase mTOR more than
acute exercise alone and lead to enhanced protein synthesis and
muscle hypertrophy.
The increased protein synthesis with enhanced dietary amino acid
availability occurs not only because of the greater net supply of
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amino acids but also because of changes in hormonal
concentrations that create a more favorable anabolic environment.
Insulin serves as a strong anabolic stimulus for skeletal muscle
hypertrophy, as shown in figure 10.7. In the presence of adequate
substrate, insulin (which rises after a meal) is capable of stimulating
skeletal muscle protein synthesis and hypertrophy in young muscles.
RESEARCH PERSPECTIVE 10.2
Lifting Before Bedtime for Enhanced Muscle Protein
Synthesis
Ingesting protein after a bout of resistance exercise stimulates muscle protein
synthesis and inhibits muscle breakdown, resulting in an overall increase in
muscle protein content during the acute phase of recovery. Because of this
phenomenon, postexercise protein ingestion is a widely used strategy for
increasing muscle hypertrophy and speeding recovery following resistance
exercise training.
Various factors can affect postexercise protein synthesis, including the
amount, type, and timing of postexercise protein ingestion. Studies have
shown that protein ingestion before bed increases overnight amino acid
availability and stimulates muscle protein synthesis during overnight sleep.
Presleep protein supplementation increases strength and hypertrophy gains
over a prolonged resistance exercise training program, and protein ingestion
before sleep may be a practical way to support muscle mass and maximize
hypertrophy during training.
A 2016 study conducted in the Netherlands25 examined whether an acute
bout of resistance exercise performed in the evening could further increase
the muscle protein synthesis response to presleep protein ingestion.
Researchers hypothesized that by combining the powerful stimulus for
protein synthesis immediately following exercise with presleep protein
ingestion, they would see an even larger increase in new protein synthesis
overnight. To study this, the researchers recruited 24 healthy young men and
divided them into two groups: presleep protein ingestion plus evening
exercise (PRO+EX) or presleep protein alone (PRO). After a standardized
meal, the PRO+EX subjects performed 60 min of lower-body resistance
exercise while the PRO subjects rested. After the exercise or rest session, all
of the subjects consumed the same drink containing 20 g of protein. Muscle
biopsy samples were taken, and a labeled amino acid isotope was continually
infused for the measurement of protein turnover. Just before bed, each
subject ingested another 30 g of labeled protein. Overnight, blood samples
were collected at 30, 60, 90, 150, 210, 330, and 450 min while the subject
slept, and a second muscle biopsy was obtained the following morning.
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The results showed that overnight protein synthesis of the myofibrils was
~35% greater in the PRO+EX subjects compared to the PRO subjects. In
addition, much more of the labeled dietary protein-derived amino acids were
incorporated into the new myofibrils of the PRO+EX overnight. These
findings led the study team to conclude that resistance exercise performed in
the evening increases the overnight muscle protein synthesis response to
presleep protein ingestion. Therefore, combining protein ingestion before
sleep with resistance exercise may be a useful strategy when trying to
maximize skeletal muscle reconditioning overnight.
Insulin stimulates protein synthesis from available amino acids by
promoting a more efficient conversion of genetic codes carried by
mRNA into proteins, a process known as translation. This process is
accomplished by cellular organelles known as ribosomes, so it
stands to reason that increasing ribosome content in the muscle
fibers (that is, increasing the translational capacity) will also result in
more protein being synthesized. Ribosome biogenesis, the creation
of new ribosomes, appears to be an important mechanism regulating
muscle size in response to resistance exercise. In fact, when the
synthesis of new ribosomes is blocked biochemically, muscles fail to
undergo hypertrophy. Notably, recent studies show that mTOR is
involved in the synthesis of ribosomes in the cell nucleus in addition
to its role in regulating translation in the cytoplasm (figure 10.7),
which puts this kinase at center stage in the muscle growth process.
FIGURE 10.7 Schematic representation of the separate and combined roles of resistance training,
insulin, and amino acid intake on skeletal muscle protein synthesis.
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Redrawn from Dickinson et al. (2013).
In Review
Resistance exercise and protein intake are powerful stimulators of skeletal
muscle protein synthesis.
Resistance-trained athletes should consume an adequate amount of high-quality
protein (as high as 1.7 g per kg of body weight per day) along with carbohydrate
in order to stimulate muscle protein synthesis and also replenish muscle
glycogen stores after exercise.
The rate of protein synthesis within the myofibrils is controlled primarily by an
enzyme known as mTOR. The primary stimulus for protein synthesis is the
mechanical stretch applied to the muscle, which activates mTOR through a
signaling pathway involving IGF-1.
Ribosome biogenesis, the creation of new ribosomes, appears to be another
important mechanism regulating muscle hypertrophy in response to resistance
exercise.
Resistance Training for Special Populations
Until the 1970s, resistance training was widely regarded as
appropriate only for young, healthy male athletes. This narrow
concept led many people to overlook the benefits of resistance
training when planning their own activities. In recent years,
considerable interest has focused on training for women, children,
and people who are elderly. As mentioned earlier in this chapter, the
widespread use of resistance training by women, either for sport or
for health-related benefits, is rather recent. Substantial knowledge
has developed since the early 1970s revealing that women and men
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have the same ability to develop strength but that, on average,
women may not be able to achieve peak values as high as those
attained by men. This difference in strength is attributable primarily
to muscle size differences related to sex differences in anabolic
hormones. Resistance training techniques developed for and applied
to men’s training seem equally appropriate for women’s training.
Issues of strength and resistance training for women are covered in
more detail in chapter 19. In this section, we first consider age, and
then we summarize the importance of this form of training for all
athletes, regardless of their sex, age, or sport.
Relative gains in strength appear to be similar when we compare
women to men, children to adults, and elderly people to young and
middle-aged adults when these gains are expressed as a
percentage of their initial strength. However, the increase in the
absolute weight lifted is generally greater in men compared to
women, in adults compared to children, and in young adults
compared to older adults. For example, after 20 weeks of resistance
training, assume that a 12-year-old boy and a 25-year-old man each
improves his bench press strength by 50%. If the man’s initial bench
press strength (1-repetition maximum, 1RM) were 50 kg (110 lb), he
would have improved by 25 kg (55 lb) to a new 1RM of 75 kg (165
lb). If the boy’s initial 1RM were 25 kg, he would have improved by
12.5 kg (28 lb) to a new 1RM of 37.5 kg (83 lb).
Resistance Exercise for Older Adults
Interest in resistance training for elderly people has increased since
the 1980s. A substantial loss of fat-free body mass accompanies
aging, a condition known as sarcopenia. This loss reflects mainly
the loss of muscle mass, largely because most people become less
active as they age. When a muscle isn’t used regularly, it loses
function, with predictable atrophy and loss of strength.
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Can resistance training in elderly people prevent or reverse this
process, and does nutrition play the same role in older people as it
does in young individuals? Elderly exercisers can indeed gain
strength and muscle mass in response to resistance training. This
fact has important implications for both their health and quality of life
(discussed in chapter 18). One of the important benefits is that, with
maintained or improved strength, they are less likely to fall. This is
significant because falls are a major source of injury and debilitation
for elderly people and often lead to death.
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Under basal conditions, fractional protein synthesis and
breakdown are not much different between young and aged people.
Rather, sarcopenia results from aged muscle’s inability to respond
appropriately to anabolic stimuli. An acute bout of resistance
exercise does not appear to elicit the same hypertrophic response in
skeletal muscles of older individuals. This anabolic resistance has
been attributed to the inability of resistance exercise to appropriately
increase mTOR signaling in the elderly.5 Resistance training is
certainly capable of increasing strength and muscle mass in elderly
persons; the response is simply blunted. With resistance training,
large increases in strength are often accompanied by only small
increases in myofibrillar protein and muscle size. In this age group,
strength increases depend significantly on neural adaptations.
The impact of protein intake on muscle hypertrophy in the elderly
is likewise blunted. Whereas as little as 5 g of protein in combination
with resistance training stimulates skeletal muscle protein synthesis
in young individuals, larger amounts must be ingested to cause the
same effect in the elderly. This may be attributable to changes in the
sensitivity of aged muscle to branched-chain amino acids. Studies
indicate that ingestion of 25 to 30 g of high-quality protein or greater
than 2 g of leucine is necessary to stimulate aged muscle protein
synthesis to a similar degree as in young muscle. Aging is also
associated with a resistance of skeletal muscle to the influence of
insulin on protein synthesis, which could be a key factor in the
etiology of sarcopenia.
In human aging, there is significant variation in regional body
composition, and age-associated dysfunction and disability have
been associated with sex and race. For example, women have
greater muscle fat infiltration and higher subcutaneous fat and lower
limb mass compared to men, and African Americans exhibit greater
limb muscle mass that is accompanied by greater subcutaneous fat
and inter- and intramuscular fat than Caucasians of the same sex.
Are there sex- and race-based differences in the physiological
adaptations to resistance training in middle-aged and older adults? A
study conducted at the University of Maryland used a unique one-leg
strength training protocol to examine the influence of sex and race
on thigh muscle volume, subcutaneous fat, and intermuscular fat
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changes in response to resistance training.27 Subjects, which
included Caucasian and African American men and women aged 50
to 85 years, completed 10 weeks of unilateral knee extension
training.
All groups had an increase in thigh muscle volume of the
exercised leg. While the men experienced a greater absolute
increase in muscle size, when the data were represented as a
percentage increase, changes in muscle volume were similar
between men and women. Nor were there any sex differences with
respect to changes in subcutaneous fat or intermuscular fat. There
were no differences in muscle or fat adaptations to training between
Caucasian and African American exercisers. The results of this study
indicate that strength training does not alter subcutaneous or
intermuscular fat, regardless of sex or race. Given that there do
appear to be racial differences in the incidence of metabolic
disorders and functional measures of muscle quality among the
elderly, other unexplored factors likely explain the racial disparity.
Resistance Training for Children
The wisdom of resistance training for children and adolescents has
long been debated. The potential for injury, particularly growth plate
injuries from the use of free weights, has caused much concern.
Many people once believed that children would not benefit from
resistance training, based on the assumption that the hormonal
changes associated with puberty are necessary for gaining muscle
strength and mass. We now know that children and adolescents can
train safely with minimal risk of injury if appropriate safeguards are
implemented. Furthermore, they can indeed gain both muscular
strength and muscle mass.
Resistance training programs for children should be prescribed in
much the same way as for adults, but with a special emphasis on
teaching proper lifting technique. Specific guidelines have been
established by a number of professional organizations, including the
American Orthopaedic Society for Sports Medicine, the American
Academy of Pediatrics, the American College of Sports Medicine,
the National Athletic Trainers’ Association, the National Strength and
Conditioning Association, the President’s Council on Physical
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Fitness and Sports, and the U.S. Olympic Committee. Basic
guidelines for the progression of resistance exercise in children are
presented in table 10.1.
TABLE 10.1 Basic Guidelines for Resistance Exercise
Progression in Children
Age
Considerations
7 years or younger
Introduce child to basic exercises using little or no weight; develop the concept of a training
session; teach exercise technique; progress from body weight calisthenics, partner exercises,
and lightly resisted exercises; keep volume low.
Gradually increase the number of exercises; practice exercise technique in all lifts; start gradual
progressive loading of exercises; keep exercises simple; gradually increase training volume;
carefully monitor tolerance of the exercise stress.
Teach all basic exercise techniques; continue progressive loading of each exercise; emphasize
exercise techniques; introduce more advanced exercises with little or no resistance. Progress to
more advanced youth programs in resistance exercise; add sport-specific components;
emphasize exercise techniques; increase volume.
Progress to more advanced youth programs in resistance exercise; add sport-specific
components; emphasize exercise techniques; increase volume.
Move child to entry-level adult programs after all background knowledge has been mastered and
a basic level of training experience has been gained.
8-10 years
11-13 years
14-15 years
16 years or older
Note. If a child of any age begins a program with no previous experience, start the child at the level for the previous age category
and move him or her to more advanced levels as exercise toleration, skill, amount of training time, and understanding permit.
Reprinted by permission from W.J. Kraemer and S.J. Fleck, Strength Training for Young Athletes, 2nd ed. (Champaign, IL: Human Kinetics,
2005), 5.
Resistance Training for Athletes
Gaining strength, power, or muscular endurance simply for the sake
of being stronger, being more powerful, or having greater muscular
endurance is of relatively little importance to athletes unless it also
improves their athletic performance. Resistance training by fieldevent athletes and competitive weightlifters makes intuitive sense.
The need for resistance training by the gymnast, distance runner,
baseball player, high jumper, or ballet dancer is less obvious.
RESEARCH PERSPECTIVE 10.3
Resistance Training Can Improve Health Without
Changing BMI
Childhood obesity has increased dramatically over the last decade, and
obese adolescents are significantly more likely to have metabolic and
cardiovascular disease. Regular physical activity improves metabolic and
cardiovascular health, and increasing aerobic activity is often recommended
to reduce the risk of disease in obese individuals. It is well documented that
aerobic training improves blood flow responses, reduces resting blood
pressure, reduces inflammation, increases insulin sensitivity, and improves
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body composition in overweight and obese individuals. However, adherence
to aerobic training programs is very low in this unfit population. Resistance
training could be an alternative strategy to improve health while increasing
adherence in obese individuals. Most studies to date that have investigated
resistance training to improve cardiovascular and metabolic outcomes in
obesity have combined resistance training with aerobic training; because of
this, little is known about the isolated effects of resistance exercise training
on cardiovascular and metabolic health in obesity.
In 2015, a group of exercise physiologists in Brazil conducted a study to
investigate the effects of a supervised resistance exercise training program
on measures of metabolic and cardiovascular health in obese adolescents.4
Twenty-four obese adolescents (mean age of 14 years) performed 12 weeks
of supervised resistance exercise training that included all major muscle
groups. Body mass index, body composition, blood pressure, endothelial
function (a measure of blood vessel health), inflammation, and insulin
resistance were measured before and after training. Despite that fact that the
body mass index (BMI) did not change, study participants had significantly
lower body fat and waist circumferences after the 12 weeks of training. Blood
pressure, endothelial function, inflammation, insulin resistance, and
performance on a submaximal exercise test all improved as well.
Overall, the findings from this study led to the conclusion that resistance
training improves cardiovascular and metabolic health in obese adolescents,
even if BMI does not change. Although there were no changes in body mass,
endothelial function, blood pressure, and metabolic profiles all improved.
Resistance training programs may be an effective alternative to aerobic
training to reduce the risk of cardiovascular and metabolic disease and may
increase adherence to exercise programs in obese adolescents.
We do not have extensive research to document the specific
benefits of resistance training for every sport or for every event
within a sport. But clearly, each has basic strength, power, and
muscular endurance requirements that must be met to achieve
optimal performance. Training beyond these requirements, however,
may be unnecessary.
Training is costly in terms of time, and athletes can’t afford to
waste time on activities that won’t result in better athletic
performances. Thus, some performance measurement is imperative
to evaluate any resistance training program’s efficacy. To resistance
train solely to become stronger, with no associated improvement in
performance, is of questionable value. However, it should also be
recognized that resistance training to improve muscular endurance
581
can reduce the risk of injury for most sports because fatigued
individuals are at an increased risk of injury.
In Review
Resistance training can benefit almost everyone, regardless of the person’s sex,
age, or athletic involvement.
In elderly people, resistance training can slow or reverse the age-associated loss
of muscle mass known as sarcopenia.
Aged skeletal muscle retains the ability to respond to exercise, insulin, and
enhanced protein intake to substantially increase net protein synthesis. However,
older muscles have a blunted response compared to young muscles.
Most athletes in most sports can benefit from resistance training if an appropriate
program is designed for them. But to ensure that the program is working,
performance should be assessed periodically and the training regimen adjusted
as needed.
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IN CLOSING
In this chapter, we have considered the role of resistance training in increasing
muscular strength and improving performance. We have examined how muscle
strength is gained through both muscular and neural adaptations, the
importance of dietary protein intake in muscle hypertrophy, how resistance
training can slow the impact of sarcopenia in the elderly, and how resistance
training is of importance for both health and sport, regardless of age or sex. In
the next chapter, we turn our attention away from resistance training and begin
exploring how the body adapts to aerobic and anaerobic training.
KEY TERMS
atrophy
autogenic inhibition
chronic hypertrophy
fiber hyperplasia
fiber hypertrophy
mTOR
resistance training
sarcopenia
transient hypertrophy
STUDY QUESTIONS
1.
What is a reasonable expectation for percentage strength gains following a
6-month resistance training program? How do these percentage gains
differ by age, sex, and previous resistance training experience?
2.
What is the suggested minimal intensity for resistance training that will
lead to muscle hypertrophy when the exercises are performed to volitional
fatigue?
3.
Discuss the different theories that have attempted to explain how muscles
gain strength with training.
4.
What is autogenic inhibition? How might it be important to resistance
training?
5.
6.
Differentiate between transient and chronic muscle hypertrophy.
7.
What is the physiological basis for hypertrophy?
What is fiber hyperplasia? How might it occur? How might it be related to
gains in size and muscle strength with resistance training?
583
8.
Describe the respective effects of intensity and circulating hormones on
muscle adaptation to fatiguing resistance training.
9.
10.
What is the physiological response to muscle immobilization?
11.
Is there an optimal timing of protein ingestion when an individual is trying
to optimize the hypertrophic response to successive exercise sessions?
12.
What is the role of mTOR in protein synthesis? How are ribosomes
involved in the process?
13.
How do the basic guidelines for prescribing resistance exercise for children
differ from those for adults?
To support protein synthesis during resistance training, what type of
protein should be ingested and how much?
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter
QUIZ tests your understanding of the material covered in the chapter.
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585
11
Adaptations to Aerobic and Anaerobic
Training
In this chapter and in the web study guide
Adaptations to Aerobic Training
Muscular Versus Cardiorespiratory Endurance
Evaluating Cardiorespiratory Endurance Capacity
Cardiovascular Adaptations to Training
Respiratory Adaptations to Training
Adaptations in Muscle
Metabolic Adaptations to Training
Integrated Adaptations to Chronic Endurance Exercise
What Limits Aerobic Power and Endurance Performance?
Long-Term Improvement in Aerobic Power and Cardiorespiratory Endurance
Factors Affecting an Individual’s Response to Aerobic Training
Cardiorespiratory Endurance in Nonendurance Sports
Aerobic Deconditioning
VIDEO 11.1 presents Ben Levine on the significance of
O2max for sport performance.
AUDIO FOR FIGURE 11.7 describes how the variables of maximal cardiac output and red blood cell
volume impact
O2max values in individuals.
AUDIO FOR FIGURE 11.8 describes the increases in total blood volume and plasma volume with
endurance training.
ACTIVITY 11.1 Adaptations reviews the cardiovascular, respiratory, and metabolic responses to training.
AUDIO FOR FIGURE 11.15 describes a twin study on the effect of heredity on
O2max.
ACTIVITY 11.2 Individual Response considers the factors affecting individual response to training.
ACTIVITY 11.3 Aerobic Training explores adaptations in response to aerobic training by applying them
to real-life situations.
Adaptations to Anaerobic Training
Changes in Anaerobic Power and Anaerobic Capacity
Adaptations in Muscle with Anaerobic Training
586
Adaptations in the Energy Systems
ACTIVITY 11.4 Anaerobic Training explores adaptations in response to anaerobic training by applying
them to real-life situations.
Adaptations to High-Intensity Interval Training
Specificity of Training and Cross-Training
In Closing
ACTIVITY 11.5 Putting It All Together reviews all concepts related to adaptations to aerobic and
anaerobic training.
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O
n October 8, 2016, the Ironman World Championships were held in Kona,
on the Big Island of Hawaii, for the 40th time. Organized by the World Triathlon
Corporation, professional triathletes qualified for the race based on a point system
and a total of $650,000 in prize money was awarded. German athlete Jan Frodeno
completed this grueling event in 8:06:30 to win his second World Championship in
as many years, completing the 3.9 km (2.4 mi) swim through tough ocean waves in
just over 48 min, biking 180 km (112 mi) through hot lava fields in under 4.5 h, then
running 42 km (26.2 mi) in 2:45:34. In the women’s division, Daniela Ryf of
Switzerland earned her second (and back-to-back) Ironman title, finishing almost 24
min ahead of the next closest woman competitor in 8:46:46—the sole woman’s
performance under 9 h. How are these athletes able to compete in this race? While
there is little doubt that they are genetically gifted—including a high O2max—
rigorous sport-specific training is also required to develop their cardiorespiratory
endurance capacities.
During a single bout of aerobic exercise, the human body precisely
adjusts its cardiovascular and respiratory function to meet the energy
and oxygen demands of actively contracting muscle. When these
systems are challenged repeatedly, as happens with regular exercise
training, they adapt in ways that allow the body to improve O2max
and overall endurance performance. Aerobic training, or
cardiorespiratory endurance training, improves cardiac function and
peripheral blood flow and enhances the capacity of the muscle fibers
to generate greater amounts of adenosine triphosphate (ATP). In this
chapter, we examine adaptations in cardiorespiratory function in
response to endurance training and how such adaptations improve
an athlete’s endurance capacity and performance. Additionally, we
examine adaptations to anaerobic training. Anaerobic training
improves anaerobic metabolism; short-term, high-intensity exercise
capacity; tolerance for acid–base imbalances; and in some cases,
muscle strength. Both aerobic and anaerobic training induce a variety
of adaptations that benefit exercise and sport performance.
The effects of training on cardiovascular and respiratory, or
aerobic, endurance are well known to endurance athletes like
distance runners, cyclists, cross-country skiers, and swimmers but
588
are often ignored by other types of athletes. Training programs for
many nonendurance athletes often ignore the aerobic endurance
component. This is understandable, because for maximum
improvement in performance, training should be highly specific to the
particular sport or activity in which the athlete participates, and
endurance is frequently not recognized as important to nonendurance
activities. The reasoning is, why waste valuable training time if the
result is not improved performance?
The problem with this reasoning is that most nonendurance sports
do indeed have an endurance, or aerobic, component. For example,
in football, players and coaches might fail to recognize the
importance of cardiorespiratory endurance as part of the total training
program. From all outward appearances, American football is an
anaerobic, or burst-type, activity consisting of repeated bouts of highintensity work of short duration. Seldom does a run exceed 40 to 60
yd (37-55 m), and even this is usually followed by a substantial rest
interval. The need for endurance may not be readily apparent. What
athletes and coaches might fail to consider is that this burst-type
activity must be repeated many times during the game. With a higher
aerobic endurance capacity, an athlete could maintain the quality of
each burst activity throughout the game and would still be relatively
fresh (less drop-off in performance, fewer feelings of fatigue) during
the all-important closing minutes of the game.
Chapters 9 and 14 cover the principles of training for sport
performance—the “how,” “when,” and “how much” questions about
how training improves athletic performance. The focus here is on
those physiological changes that occur within the body systems when
aerobic or anaerobic exercise is repeated regularly to induce a
training response.
Adaptations to Aerobic Training
Improvements in endurance that accompany regular (e.g., daily,
every other day) aerobic training, such as running, cycling, or
swimming, result from multiple adaptations to the training stimuli.
Some adaptations occur in the cardiovascular system, improving
circulation to and within the muscles. Still other important changes
occur within the muscles themselves, promoting more efficient
589
utilization of oxygen and fuel substrates. Pulmonary adaptations, as
will be noted later, occur to a lesser extent.
Muscular Versus Cardiorespiratory Endurance
Endurance is a term that refers to two separate but related concepts:
muscular endurance and cardiorespiratory endurance. Each makes a
unique contribution to athletic performance, and each differs in its
importance to different athletes.
For sprinters, endurance is the quality that allows them to sustain a
high speed over the full distance of, for example, a 100 m or 200 m
dash. This component of fitness is termed muscular endurance, the
ability of a single muscle or muscle group to maintain high-intensity,
repetitive, or static contractions. This type of endurance is also
exemplified by a weightlifter doing multiple repetitions, a boxer, or a
wrestler. The exercise or activity can be rhythmic and repetitive in
nature, such as multiple repetitions of the bench press for the
weightlifter and jabbing for the boxer. Or the activity can be more
static, such as a sustained muscle action when a wrestler attempts to
pin an opponent. In either case, the resulting fatigue is confined to a
specific muscle group, and the activity’s duration is usually no more
than 2 min. Muscular endurance is highly related to muscular strength
and to anaerobic power development.
While muscular endurance is specific to individual muscles or
muscle groups, cardiorespiratory endurance relates to the ability to
sustain prolonged, dynamic whole-body exercise using large muscle
groups. Cardiorespiratory endurance is related to the development of
the cardiorespiratory systems’ ability to maintain oxygen delivery to
working muscles during prolonged exercise, as well as the muscles’
ability to use energy aerobically (discussed in chapters 2 and 5). This
is why the terms cardiorespiratory endurance and aerobic endurance
are sometimes used synonymously.
Evaluating Cardiorespiratory Endurance Capacity
Studying the effects of training on endurance requires an objective,
repeatable means of measuring an individual’s cardiorespiratory
endurance capacity. In that way, the exercise scientist, coach, or
athlete can monitor improvements as physiological adaptations occur
during the training program.
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Maximal Endurance Capacity:
O2max
Most exercise scientists regard O2max, sometimes called maximal
aerobic power or maximal aerobic capacity, as the best objective
laboratory measure of cardiorespiratory endurance. Recall from
chapter 5 that O2max is defined as the highest rate of oxygen
consumption attainable during maximal or exhaustive exercise.
O2max as defined by the Fick equation is determined by maximal
cardiac output (delivery of oxygen and blood flow to working muscles)
and the maximal (a- )O2 difference (the ability of the active muscles
to extract and use the oxygen).
As exercise intensity increases, oxygen consumption eventually
either plateaus or decreases slightly, even with further increases in
workload, indicating that a true maximal O2max has been achieved.
With endurance training, more oxygen can be delivered to, and
used by, active muscles than in an untrained state. Previously
untrained subjects demonstrate average increases in O2max of 15%
to 20% after a 20-week training program. These improvements allow
individuals to perform endurance activities at a higher intensity,
improving their performance potential. Figure 11.1 illustrates the
increase in O2max after 12 months of aerobic training in a previously
untrained individual. In this example, O2max increased by about 30%.
Note that the O2 cost of running at a certain submaximal intensity
(referred to as running economy) did not change, but higher running
speeds could be attained after training.
VIDEO 11.1 Presents Ben Levine on the significance of O2max for
sport performance.
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Submaximal Endurance
FIGURE 11.1 Changes in
kg−1
O2max with 12 months of endurance training.
O2max increased from 44 to
min−1,
57 ml ·
·
a 30% increase. Peak speed during the treadmill test increased from 13 km/h (8
mph) to 16 km/h (~10 mph).
In addition to increasing maximal endurance capacity, endurance
training also increases submaximal endurance, which is more
difficult to evaluate. A lower steady-state heart rate at the same
submaximal exercise intensity is one physiological variable that can
be used to objectively quantify the effect of training. Additionally, one
could measure the average peak absolute power output a person can
maintain over a fixed period of time on a cycle ergometer. For
running, the average peak speed or velocity a person can maintain
for a set period of time would be a similar test of submaximal
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endurance. Generally, these tests last 30 min to an hour and reflect
the concept of critical power discussed in chapter 5. Submaximal
endurance, like critical power, is more closely related to actual
competitive endurance performance than O2max. With endurance
training, submaximal endurance increases.
RESEARCH PERSPECTIVE 11.1
How Much Can
O2max Improve?
In 1968, the Dallas bed-rest study demonstrated that O2max could be doubled
(from roughly 25 ml · kg−1 · min−1 to 50 ml · kg−1 · min−1) within a few weeks of
training after a period of detraining.30 Despite this huge increase in O2max
following bed-rest induced detraining, 50 ml · kg−1 · min−1 is a rather typical
O2max for a recreational endurance athlete, and it is unlikely that an average
active adult can increase O2max from this average to values even remotely
close to double.21 Meanwhile, elite endurance athletes typically have O2max
values approaching 80 ml · kg−1 · min−1, with the highest value ever published
at an incredible 90.6 ml · kg−1 · min−1 in an Olympic gold medalist crosscountry skier. It is unlikely that any ordinary human can achieve such
astounding values even with rigorous training programs, so how, and by how
much, can O2max actually be enhanced?
Large O2max changes may take years to achieve. Prospective training
studies are challenging to undertake in the laboratory, but the longest
published study showed only a 21% increase in O2max over 12 months of
training at moderate to high intensities every other day. Other training studies
lasting 4 to 6 months show even more modest increases of 9% to 17%, and
overall it appears that average endurance training improves O2max ~0.5
L/min. High-intensity interval training has shown the largest increase in O2max
(44%), but it should be noted that the training intensities and volumes in all of
these studies are far lower than the training load of world-class athletes. In
contrast to the average-fit subjects in these longitudinal studies, young (15-25
years of age) world-class athletes can substantially increase their O2max from
an already high 55 to 60 ml · kg−1 · min−1 to 75 to 80 ml · kg−1 · min−1 with
years of intense training. This phenomenon suggests that large increases in
O2max can be seen in athletes undergoing intense training and that training in
early life is likely a determinant of very high O2max values recorded in
endurance champions.
A high O2max is the product of a high maximal cardiac output ( max) and
a high oxygen-carrying capacity of the blood. This maximal blood flow and
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oxygen carrying leads to increased oxygen delivery to the exercising muscles.
The high
max in elite athletes is the result of increased stroke volume, since
maximal heart rate does not change with training. Endurance trained athletes
achieve this higher stroke volume through changes in the left ventricle of the
heart such that it has a larger mass and is more distensible and therefore
easier to fill with each heartbeat. But what about nonelite athletes? It remains
unknown if average individuals can ever reach
max values observed in elite
athletes. The initial increase in stroke volume observed with training healthy,
normal volunteers is due to an increased blood volume rather than changes in
the myocardium. After 1 year of exercise training in previously untrained
individuals, left ventricle mass has been shown to increase. However, these
changes do not result in very large increases in
max. These findings suggest
that it is unlikely that individuals with average cardiac function can ever reach
values observed in elite athletes, but it may be that exercise training during
childhood and early adulthood may favor the development of these
advantageous cardiac characteristics.
Given the limited potential for training to increase
max, the adaptation for
improved oxygen delivery is an important factor for the improvement of O2max
with endurance training. Oxygen-carrying capacity is directly related to the
number of hemoglobin available to bind to oxygen, and hemoglobin mass
correlates tightly with exercise performance. There is little doubt that exercise
training increases hemoglobin mass or total red blood cell volume ~20%. It is
unknown if long-term endurance training can increase hemoglobin mass from
normal values (~700 g) to that observed in elite athletes (~1,200 g), but it
appears unlikely. There may be genetic determinants of total hemoglobin
mass, but research has thus far failed to find a genetic polymorphism to
explain extremely high hemoglobin mass in elite athletes.
Finally, improvements in oxygen extraction, i.e., increases in (a-v)O2
difference, may also contribute to the increase in
O2max with training.
Athletes have a more homogeneous blood flow distribution during submaximal
exercise, which results in a higher oxygen extraction compared to untrained
individuals. Systemic maximal oxygen extraction can be improved with training
in healthy volunteers, from 72% up to 84%. Although this is a meaningful
improvement, it is still nowhere near oxygen extraction reported in elite
endurance athletes (93%). It is unlikely that average individuals can achieve
the high oxygen extractions observed in elite athletes; however, the possibility
that already trained elite endurance athletes can further improve oxygen
extraction has yet to be studied.
Overall, although endurance training leads to improvements in the
mechanisms contributing to O2max, the overall increases observed in healthy,
normal individuals rarely exceed 0.5 L/min and never reach the extraordinarily
high values observed in elite endurance athletes. Even highly trained athletes
seem to plateau after age 25, and increases in performance after that are due
to increases in other mechanisms such as mechanical efficiency or critical
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power. O2max is a powerful determinant of endurance performance, but the
magnitude of improvements that can be achieved through training are
relatively small, even in elite endurance athletes.20
Cardiovascular Adaptations to Training
Multiple cardiovascular adaptations occur in response to exercise
training, including changes in the following:
Heart size
Stroke volume
Heart rate
Cardiac output
Blood flow
Blood and red cell volumes
Not surprisingly, these variables are interrelated. For example,
training-induced increases in stroke volume depend on increases in
both heart size and blood volume. To fully understand adaptations in
these variables, it is important to review how these components relate
to oxygen transport.
Oxygen Transport System
Cardiorespiratory endurance is related to the cardiovascular and
respiratory systems’ ability to deliver sufficient oxygen to meet the
needs of metabolically active tissues.
Recall from chapter 8 that the ability of the cardiovascular and
respiratory systems to deliver oxygen to active tissues is defined by
the Fick equation, which states that whole-body oxygen
consumption is determined by both the delivery of oxygen via blood
flow (cardiac output) and the amount of oxygen extracted by the
tissues, the (a- )O2 difference. The product of cardiac output and the
(a- )O2 difference determines the rate at which oxygen is being
consumed:
O2 = stroke volume × heart rate × (a- )O2 difference
and
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O2max = maximal stroke volume × maximal heart rate × maximal (a)O2 difference
Because maximal heart rate (HRmax) either stays the same or
decreases slightly with training, increases in
O2max depend on
adaptations in maximal stroke volume and maximal (a- )O2
difference.
The oxygen demand of exercising muscles increases with
increasing exercise intensity. Aerobic endurance depends on the
cardiorespiratory system’s ability to deliver sufficient oxygen to these
active tissues to meet their heightened demands for oxygen for
oxidative metabolism. As maximal levels of exercise are achieved,
heart size, blood flow, blood pressure, and blood volume can all
potentially limit the maximal ability to transport oxygen. Endurance
training elicits numerous changes in these components of the
oxygen transport system that enable it to function more effectively.
Heart Size
The measurement of heart size has been of interest to cardiologists
for years because a hypertrophied, or enlarged, heart is typically a
pathological condition indicating the presence of cardiovascular
disease. Clinicians and scientists commonly use echocardiography to
accurately measure the size of the heart and its chambers.
Echocardiography involves the technique of ultrasound, which uses
high-frequency sound waves directed through the chest wall to the
heart. These sound waves are emitted from a transducer placed on
the chest; once they contact the various structures of the heart, they
rebound back to a sensor, which is able to capture the deflected
sound waves and provide a moving picture of the heart. A trained
physician or technician can visualize the size of the heart’s chambers,
thicknesses of its walls, and heart valve action. There are several
forms of echocardiography: M-mode echocardiography, which
provides a one-dimensional view of the heart; two-dimensional
echocardiography; and Doppler echocardiography, which is used
more often to measure blood flow through large arteries.
As an adaptation to the increased work demand, cardiac muscle
mass and ventricular volume increase with training. Cardiac muscle,
like skeletal muscle, undergoes morphological adaptations as a result
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of chronic endurance training. At one time, cardiac hypertrophy
induced by exercise—athlete’s heart, as it was called—was viewed
with concern because experts incorrectly believed that enlargement
of the heart always reflected a pathological state, as sometimes
occurs with severe hypertension. Training-induced cardiac
hypertrophy, on the other hand, is now recognized as a normal
adaptation to chronic endurance training.
The left ventricle, as discussed in chapter 6, does the most work
and thus undergoes the greatest adaptation in response to
endurance training. The type of ventricular adaptation depends on the
type of exercise training performed. For example, during resistance
training, the left ventricle must contract against increased afterload
from the systemic circulation. From chapter 8 we learned that blood
pressure during resistance exercise can exceed 480/350 mmHg. This
presents a considerable resistance that must be overcome by the left
ventricle. To overcome this high afterload, the heart muscle
compensates by increasing left ventricular wall thickness, thereby
increasing its contractility. Thus, the increase in its muscle mass is in
direct response to repeated exposure to the increased afterload with
resistance training. However, there is little change in ventricular
volume.
With endurance training, left ventricular chamber size increases.
This allows for increased left ventricular filling and consequently an
increase in stroke volume. The increase in left ventricular dimensions
is largely attributable to a training-induced increase in plasma volume
(discussed later in this chapter) that increases left ventricular enddiastolic volume (increased preload). In concert with this, a decrease
in heart rate at rest caused by increased parasympathetic tone, and
during exercise at the same rate of work, allows a longer diastolic
filling period. The increases in plasma volume and diastolic filling time
increase left ventricular chamber size at the end of diastole. This
effect of endurance training on the left ventricle is often called a
volume loading effect.
It was originally hypothesized that this increase in left ventricular
dimensions was the only change in the left ventricle caused by
endurance training. Additional research has revealed that, similar to
what happens in resistance training, myocardial wall thickness
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increases with endurance training. Highly trained endurance athletes
(competitive cross-country skiers, endurance cyclists, and longdistance runners) have greater left ventricular masses than non–
endurance-trained men and women. Furthermore, left ventricular
mass is highly correlated with O2max.
Fagard12 conducted the most extensive review of the existing
research literature in 1996, focusing on long-distance runners (135
athletes and 173 controls), cyclists (69 athletes and 65 controls), and
strength athletes (178 athletes, including weight- and powerlifters,
bodybuilders, wrestlers, throwers, and bobsledders, and 105
controls). For each group, the athletes were matched by age and
body size with a group of sedentary control subjects. For each group
of runners, cyclists, and strength athletes, the internal diameter of the
left ventricle (LVID, an index of chamber size) and the total left
ventricular mass (LVM) were greater in the athletes compared with
their age- and sized-matched controls (figure 11.2). Thus, data from
this review support the hypothesis that both left ventricular chamber
size and wall thickness increase with endurance training.
Most studies of heart size changes with training have been crosssectional, comparing trained individuals with sedentary, untrained
individuals. Certainly a portion of the differences that we see in figure
11.2 can be attributed to genetics, not training. However, a number of
longitudinal studies have followed individuals from an untrained state
to a trained state, and others have followed individuals from a trained
state to an untrained state. These studies have reported increases in
heart size with training and decreases with detraining. Therefore,
training does bring about changes, but they are likely not as large as
the differences shown in figure 11.2.
In Review
Cardiorespiratory endurance (also called maximal aerobic power) refers to the
ability to perform prolonged, dynamic exercise using a large muscle mass.
O2max—the highest rate of oxygen consumption obtainable during maximal or
exhaustive exercise—is the best single measure of cardiorespiratory endurance.
Cardiac output, the product of heart rate and stroke volume, represents how much
blood leaves the heart each minute, whereas (a- O2 difference is a measure of
how much oxygen is extracted from the blood by the tissues. According to the
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Fick equation, the product of these values is the rate of oxygen consumption:
= stroke volume × heart rate × (a- O2 difference.
O2
Of the chambers of the heart, the left ventricle adapts the most in response to
endurance training.
With endurance training, the internal dimensions of the left ventricle increase,
mostly in response to an increase in ventricular filling secondary to an increase in
plasma volume.
Left ventricular wall thickness and mass also increase with endurance training,
allowing for a greater force of contraction.
Stroke Volume
Stroke volume at rest is substantially higher after an endurance
training program than it is before training. This endurance training–
induced increase is also seen at a given submaximal exercise
intensity and at maximal exercise. This increase is illustrated in figure
11.3, which shows the changes in stroke volume of a subject who
exercised at increasing intensities up to a maximal intensity before
and after a 6-month endurance training program. Typical values for
stroke volume at rest and during maximal exercise in untrained,
trained, and highly trained athletes are listed in table 11.1. The wide
range of stroke volume values for any given cell within this table is
largely attributable to differences in body size. Larger people typically
have larger hearts and a greater blood volume, and thus higher
stroke volumes—an important point when one is comparing stroke
volumes of different people.
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FIGURE 11.2 Percentage differences in heart size of three groups of athletes (runners, cyclists, and
strength athletes) compared with their age- and size-matched sedentary controls (0%). Percentage
differences are presented for left ventricular internal diameter (LVID), mean wall thickness (MWT), and
left ventricular mass (LVM).
Data are from Fagard (1996).
FIGURE 11.3 Changes in stroke volume with endurance training during walking, jogging, and running
on a treadmill at increasing velocities.
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TABLE 11.1 Stroke Volumes at Rest (SVrest) and During
Maximal Exercise (SVmax) for Different States of Training
Subjects
SVrest (ml/beat)
SVmax (ml/beat)
Untrained
Trained
Highly trained
50-70
70-90
90-110
80-110
110-150
150-220+
After aerobic training, the left ventricle fills more completely during
diastole. Plasma volume expands with training, which allows for more
blood to enter the ventricle during diastole, increasing end-diastolic
volume (EDV). The heart rate of a trained heart is also lower at rest
and at the same absolute exercise intensity than that of an untrained
heart, allowing more time for the increased diastolic filling. More
blood entering the ventricle increases the stretch on the ventricular
walls; by the Frank-Starling mechanism (see chapter 8), this results in
an increased force of contraction.
The thickness of the posterior and septal walls of the left ventricle
also increases slightly with endurance training. Increased ventricular
muscle mass results in increased contractile force, in turn causing a
lower end-systolic volume (ESV).
The decrease in ESV is facilitated by the decrease in peripheral
resistance that occurs with training. Increased contractility resulting
from an increase in left ventricular thickness and greater diastolic
filling (Frank-Starling mechanism), coupled with the reduction in
systemic peripheral resistance, increases the ejection fraction [equal
to (EDV − ESV) / EDV] in the trained heart. More blood enters the left
ventricle, and a greater percentage of what enters is forced out with
each contraction, resulting in an increase in stroke volume.
Adaptations in stroke volume during endurance training are
illustrated by a study in which older men trained aerobically for 1
year.10 Their cardiovascular function was evaluated before and after
training. The subjects performed running, treadmill, and cycle
ergometer exercise for 1 h each day, 4 days per week. They
exercised at intensities of 60% to 80% of O2max, with brief bouts of
exercise exceeding 90% of O2max. End-diastolic volume increased at
rest and throughout submaximal exercise. The ejection fraction
increased, which was associated with a decreased ESV, suggesting
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increased contractility of the left ventricle. O2max increased by 23%,
a substantial improvement in endurance.
To summarize, increased left ventricular dimensions, reduced
systemic peripheral resistance, and a greater blood volume account
for the increases in resting, submaximal, and maximal stroke volume
after an endurance training program.
In Review
Following endurance training, stroke volume (SV) is increased at rest and during
submaximal and maximal exercise.
A major factor leading to the SV increase is an increased end-diastolic volume
(EDV) caused by an increase in plasma volume and a greater diastolic filling time
secondary to a lower heart rate.
Another contributing factor to increased SV is an increased left ventricular force of
contraction. This is caused by hypertrophy of the cardiac muscle and increased
ventricular stretch resulting from an increase in diastolic filling (increased preload),
leading to greater elastic recoil (Frank-Starling mechanism).
Reduced systemic vascular resistance (decreased afterload) also contributes to
the increased volume of blood pumped from the left ventricle with each beat.
Heart Rate
Aerobic training has a major impact on heart rate at rest, during
submaximal exercise, and during the postexercise recovery period.
The effect of aerobic training on maximal heart rate is rather
negligible.
Resting heart rate decreases markedly as a result
of endurance training. Some studies have shown that a sedentary
individual with an initial resting heart rate of 80 beats/min can
decrease resting heart rate by approximately 1 beat/min with each
week of aerobic training, at least for the first few weeks. After 10
weeks of moderate endurance training, resting heart rate can
decrease from 80 to 70 beats/min or lower. On the other hand, wellcontrolled studies with large numbers of subjects have shown much
smaller decreases in resting heart rate, that is, fewer than 5
beats/min following up to 20 weeks of aerobic training.
Resting Heart Rate
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Recall from chapter 6 that bradycardia is a term indicating a heart
rate of fewer than 60 beats/min. In untrained individuals, bradycardia
can be the result of abnormal cardiac function or heart disease.
However, highly conditioned endurance athletes often have resting
heart rates lower than 40 beats/min, and some have values lower
than 30 beats/min. Therefore, it is necessary to differentiate between
training-induced bradycardia, which is a normal response to
endurance training, and pathological bradycardia, which can be
cause for concern.
The low resting heart rate (HR) of well-trained endurance athletes
is most often attributed to an elevated parasympathetic (vagal) tone.
However, a 2013 review of the available evidence casts doubt on this
mechanism.6 The two alternative explanations for the resting
bradycardia of athletes are a diminished sympathetic tone and a
lower intrinsic heart rate. Recall from chapter 6 that the intrinsic heart
rate is the rate of sinoatrial (SA) node firing in the absence of any
neural or hormonal input. In studies that have blocked
parasympathetic activity to the heart using the drug atropine, there is
still a significant resting bradycardia in athletes. In fact, the difference
in HR after parasympathetic blockade is greater than the difference in
the normal HR, suggesting that the bradycardia is not the result of
elevated vagal tone.
Other studies have blocked both branches of the autonomic
nervous system, that is, used a complete autonomic blockade. The
HR after complete autonomic blockade is a measure of the intrinsic
HR. In studies showing a lowered resting HR after endurance
training, the bradycardia persists after complete autonomic blockade.
Thus, the resting bradycardia seen in athletes is at least partially, and
perhaps completely, the result of a decreased intrinsic HR.
A decreased intrinsic HR can result from a remodeling of the SA
node. The SA node serves as the pacemaker of the heart due to
properties of ion channels and Ca2+-handling proteins in the SA node
cells. Changes in these properties cause the well-known
bradycardias associated with SA node disease, heart failure, atrial
fibrillation, and even aging itself. In fact, the age-associated decrease
in resting HR has been attributed to a downregulation of ryanodine
receptors (see chapter 6) that are involved in Ca2+ flux. If these
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mechanisms are involved in bradycardias associated with these other
processes and diseases, it is likely that they are involved in traininginduced bradycardia as well.
During submaximal exercise, aerobic training
results in a lower heart rate at any given absolute exercise intensity.
This is illustrated in figure 11.4, which shows the heart rate of an
individual exercising on a treadmill before and after training. At each
walking or running speed, the posttraining heart rate is lower than the
heart rate before training. The training-induced decrease in heart rate
is typically greater at higher intensities.
While maintaining a cardiac output appropriate to meet the needs
of working muscle, a trained heart performs less work (lower heart
rate, higher stroke volume) than an untrained heart at the same
absolute workload.
Submaximal Heart Rate
FIGURE 11.4 Endurance training-induced changes in heart rate during progressive walking, jogging,
and running on a treadmill at increasing speeds.
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A person’s maximal heart rate (HRmax) tends to be
stable and typically remains relatively unchanged after endurance
training. However, several studies have suggested that for people
whose untrained HRmax values exceed 180 beats/min, HRmax might be
slightly lower after training. Also, highly conditioned endurance
athletes often have lower HRmax values than untrained individuals of
the same age, although this is not always the case. Athletes over 60
years old sometimes have higher HRmax values than untrained people
of the same age.
Maximum Heart Rate
During exercise, the
product of heart rate and stroke volume provides a cardiac output
appropriate to the intensity of the activity being performed. At
maximal or near-maximal intensities, heart rate may change to
provide the optimal combination of heart rate and stroke volume to
maximize cardiac output. If heart rate is too fast, diastolic filling time is
reduced, and stroke volume might be compromised. For example, if
HRmax is 180 beats/min, the heart beats three times per second. Each
cardiac cycle thus lasts for only 0.33 s. Diastole is as short as 0.15 s
or less. This fast heart rate allows very little time for the ventricles to
fill. As a consequence, stroke volume may decrease at high heart
rates when filling time is compromised.
However, if the heart rate slows, the ventricles have longer to fill.
This has been proposed as one reason highly trained endurance
athletes tend to have lower HRmax values: Their hearts have adapted
to training by drastically increasing their stroke volumes, so lower
HRmax values can provide optimal cardiac output.
Which comes first? Does increased stroke volume result in a
decreased heart rate, or does a lower heart rate result in an
increased stroke volume? This question remains unanswered. In
either case, the combination of increased stroke volume and
decreased heart rate is a more efficient way for the heart to meet the
metabolic demands of the exercising body. The heart expends less
energy by contracting less often but more forcefully than it would if
contraction frequency were increased. Reciprocal changes in heart
rate and stroke volume in response to training share a common goal:
to allow the heart to pump the maximal amount of oxygenated blood
at the lowest energy cost.
Interactions Between Heart Rate and Stroke Volume
605
During exercise, as discussed in chapter 6, heart
rate must increase to increase cardiac output to meet the blood flow
demands of active muscles. When the exercise bout is finished, heart
rate does not instantly return to its resting level. Instead, it remains
elevated for a while, slowly returning to its resting rate. The time it
takes for heart rate to return to its resting rate is called the heart rate
recovery period.
After endurance training, as shown in figure 11.5, heart rate returns
to its resting level much more quickly after an exercise bout than it
does before training. This is true after both submaximal and maximal
exercise.
Heart Rate Recovery
FIGURE 11.5 Changes in heart rate during recovery after a 4 min, all-out bout of exercise before and
after endurance training.
Because the heart rate recovery period is shorter after endurance
training, this measurement has been proposed as an indirect index of
cardiorespiratory fitness. In general, a more fit person recovers faster
after a standardized rate of work than a less fit person, so this
measure may have some utility in field settings when more direct
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measures of endurance capacity are not possible or feasible.
However, factors other than training can also affect heart rate
recovery time. For example, an elevated core temperature or an
enhanced sympathetic nervous system response can prolong heart
rate elevation.
The heart rate recovery curve is a useful tool for tracking a
person’s progress during a training program. But because of the
potential influence of other factors, it should not be used to compare
individuals.
Cardiac Output
We have looked at the effects of training on the two components of
cardiac output: stroke volume and heart rate. While stroke volume
increases with training, heart rate generally decreases at rest and
during exercise at a given absolute intensity.
Because the magnitude of these reciprocal changes is similar,
cardiac output at rest and during submaximal exercise at a given
exercise intensity does not change much following endurance
training. In fact, cardiac output can decrease slightly. This is likely the
result of an increase in the (a- )O2 difference (reflecting greater
oxygen extraction by the tissues) or a decrease in the rate of oxygen
consumption (reflecting an increased mechanical efficiency).
Generally, cardiac output matches the oxygen consumption required
for any given intensity of effort.
Maximal cardiac output, however, increases considerably in
response to aerobic training, as seen in figure 11.6, and is largely
responsible for the increase in O2max. This increase in cardiac output
must result from an increase in maximal stroke volume, because
HRmax changes little, if any. Maximal cardiac output ranges from 14 to
20 L/min in untrained individuals and from 25 to 35 L/min in trained
individuals, and can be 40 L/min or more in highly conditioned
endurance athletes. These absolute values, however, are greatly
influenced by body size.
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FIGURE 11.6 Changes in cardiac output with endurance training during walking, then jogging, and
finally running on a treadmill as velocity increases.
Lundby and colleagues19 have argued that variability in O2max
among individuals is primarily determined by differences in two
variables: maximal cardiac output and red blood cell volume (figure
11.7). (Red cell volume changes are discussed later in this chapter.)
Therefore, the response of O2max to endurance training reflects
relative changes in these two important determinants.
FIGURE 11.7 Correlations between
volume.
O2max and (a) maximal cardiac output and (b) red blood cell
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Reprinted by permission from C. Lundby, D. Montero, and M. Joyner, “Biology of VO2 Max: Looking Under the
Physiology Map,” Acta Physiologica 220, no. 2 (2017): 218-228.
In Review
Resting heart rate decreases as a result of endurance training. In a sedentary
person, the decrease is typically about 1 beat/min per week during the initial
weeks of training, but smaller decreases have been reported. Highly trained
endurance athletes may have resting heart rates of 40 beats/min or lower.
The mechanisms responsible for the sinus bradycardia associated with endurance
training remain controversial, but likely involve both extrinsic (autonomic neural
balance) and intrinsic (SA node function) components.
Heart rate during submaximal exercise is also lower, with larger decreases seen
at higher exercise intensities.
Maximal heart rate either remains unchanged or decreases slightly with training.
Heart rate during the recovery period decreases more rapidly after training,
making it an indirect but convenient way of tracking the adaptations within an
individual that occur with training. However, this value is not useful for comparing
fitness levels of different people.
Cardiac output at rest and at submaximal levels of exercise remains unchanged
(or may decrease slightly) after endurance training.
Cardiac output during maximal exercise increases considerably and is largely
responsible for the increase in O2max. The increased maximal cardiac output is
the result of the substantial increase in maximal stroke volume, made possible by
training-induced changes in blood volume and cardiac structure and function.
Blood Flow
Active muscles need substantially more oxygen and fuel substrates
than inactive ones. To meet these increased needs, more blood must
be delivered to these muscles during exercise. With endurance
training, the cardiovascular system adapts to increase blood flow to
exercising muscles to meet their higher demand for oxygen and
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metabolic substrates. In addition to changes in the heart that allow for
better pumping and increased stroke volume, four factors account for
this enhanced blood flow to muscle following training:
Increased capillarization
Greater recruitment of existing capillaries
More effective blood flow redistribution away from inactive
regions
Increased total blood volume
To permit increased blood flow, new capillaries develop in trained
muscles. This allows the blood flowing into skeletal muscle from
arterioles to more fully perfuse the active fibers. This increase in
capillaries usually is expressed as an increase in the number of
capillaries per muscle fiber, or the capillary-to-fiber ratio. Table 11.2
illustrates the differences in capillary-to-fiber ratios between welltrained and untrained men, both before and after exercise.15
In all tissues, including muscle, not all capillaries are open at any
given time. In addition to new capillary formation, existing capillaries
in trained muscles can be recruited and open to flow, which also
increases blood flow to muscle fibers. The increase in new capillaries
with endurance training and increased capillary recruitment combine
to increase the overall area for diffusion of oxygen between the
vascular system and the metabolically active muscle fibers.
A more effective redistribution of cardiac output also can increase
blood flow to the active muscles. Blood flow is directed to the active
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musculature and shunted away from areas that do not need high flow.
Blood flow can increase to the more active fibers even within a
specific muscle group. Armstrong and Laughlin2 first demonstrated
that endurance-trained rats could redistribute blood flow to their most
active tissues during exercise better than untrained rats could. The
total blood flow to the exercising hindlimbs did not differ between the
trained and untrained rats. However, the trained rats distributed more
of their blood to the most oxidative muscle fibers, effectively
redistributing the blood flow away from the glycolytic muscle fibers.
These findings are difficult to replicate in humans because of
measurement challenges, as well as the fact that human skeletal
muscle is a mosaic with mixed fiber types among individual muscles.
Finally, the body’s total blood volume increases with endurance
training, providing more blood to meet the body’s many blood flow
needs during endurance activity without compromising venous return,
as discussed next in this chapter.
Blood Volume
Endurance training increases total blood volume, and this effect is
larger with higher training intensities. Furthermore, the effect occurs
rapidly. This increased blood volume results primarily from an
increase in plasma volume, but there is also an increase in the
volume of red blood cells. The time course and mechanism for the
increase of each of these components of blood are quite different.
The increase in plasma volume with training is thought
to result from two mechanisms. The first mechanism, which has two
phases, results in increases in plasma proteins, particularly albumin.
Recall from chapter 8 that plasma proteins are the major driver of
oncotic pressure in the vasculature. As plasma protein concentration
increases, so does oncotic pressure, and fluid is reabsorbed from the
interstitial fluid into the blood vessels. During an intense bout of
exercise, proteins leave the vascular space and move into the
interstitial space. They are then returned in greater amounts through
the lymph system. It is likely that the first phase of rapid plasma
volume increase is the result of the increased plasma albumin, which
is noted within the first hour of recovery from the first training bout. In
the second phase, protein synthesis is turned on (upregulated) by
Plasma Volume
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repeated exercise, and new proteins are formed. With the second
mechanism, exercise increases the release of antidiuretic hormone
and aldosterone, hormones that cause reabsorption of water and
sodium in the kidneys, which increases blood plasma. That increased
fluid is kept in the vascular space by the oncotic pressure exerted by
the proteins. Nearly all of the increase in blood volume during the first
2 weeks of training can be explained by the increase in plasma
volume. This early blood volume expansion allows stroke volume to
increase despite the fact that changes in the structure and function of
the heart itself take longer to develop.
An increase in red blood cell volume with endurance
training also contributes to the overall increase in blood volume
(figure 11.7b) and red cell volume, like cardiac output, is correlated to
O2max. Although the actual number of red blood cells may increase,
the hematocrit—the ratio of the red blood cell volume to the total
blood volume—may actually decrease. Figure 11.8 illustrates this
apparent paradox. Notice that the hematocrit is reduced even though
there has been a slight increase in red blood cells. A trained athlete’s
hematocrit can decrease to such an extent that the athlete appears to
be anemic on the basis of a relatively low concentration of red cells
and hemoglobin (“pseudoanemia”).
The increased ratio of plasma to cells resulting from a greater
increase in the fluid portion reduces the blood’s viscosity, or
thickness. Reduced viscosity may aid the smooth flow of blood
through the blood vessels, particularly through the smaller vessels
such as the capillaries. One of the physiological benefits of
decreasing blood viscosity is that it enhances oxygen delivery to the
active muscle mass.
Both the total amount (absolute values) of hemoglobin and the
total number of red blood cells are typically elevated in highly trained
athletes. This ensures that the blood has more than adequate
oxygen-carrying capacity; that is, the blood’s ability to deliver oxygen
to exercising muscle is not a limiting factor in exercise. The turnover
rate of red blood cells also may be higher with intense training.
Red Blood Cells
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FIGURE 11.8 Increases in total blood volume and plasma volume occur with endurance training. Note
that although the hematocrit (percentage of red blood cells) decreased from 44% to 42%, the total
volume of red blood cells increased by 10%.
In Review
Blood flow to active muscle is increased by endurance training.
Increased muscle blood flow results from four factors:
1.
2.
3.
4.
Increased capillarization
Greater opening of existing capillaries (capillary recruitment)
More effective blood flow distribution
Increased blood volume
Blood volume increases as a result of endurance training.
613
Plasma volume is expanded through increased protein content (returned from
lymph and upregulated protein synthesis). This effect is maintained and supported
by fluid-conserving hormones.
Red blood cell volume also increases, but the increase in plasma volume is
typically higher. This decreases blood viscosity, which can improve tissue
perfusion and oxygen availability.
Respiratory Adaptations to Training
No matter how proficient the cardiovascular system is at supplying
blood to exercising muscle, endurance would be hindered if the
respiratory system were not able to deliver enough oxygen to fully
oxygenate red blood cells. Respiratory system function does not
usually limit performance because ventilation can be increased to a
much greater extent than cardiovascular function. But, as with the
cardiovascular system, the respiratory system undergoes specific
adaptations to endurance training to maximize its efficiency.
Pulmonary Ventilation
After training, pulmonary ventilation is essentially unchanged at rest.
Although endurance training does not change the structure or basic
physiology of the lung, it does decrease ventilation during
submaximal exercise by as much as 30% at a given submaximal
intensity. Maximal pulmonary ventilation is substantially increased
from a rate of about 100 to 120 L/min in untrained sedentary
individuals to about 130 to 150 L/min or more following endurance
training. Breathing rates typically increase to about 180 L/min in
highly trained athletes and can exceed 200 L/min in very large, highly
trained endurance athletes. Two factors can account for the increase
in maximal pulmonary ventilation following training: increased tidal
volume and increased respiratory frequency at maximal exercise.
Ventilation is not usually a limiting factor for endurance exercise
performance. However, in some very highly trained athletes, the
pulmonary system’s capacity for oxygen transport may not be able to
meet the demands of exercising muscle and the cardiovascular
system. This results in what has been termed exercise-induced
arterial hypoxemia, in which arterial oxygen saturation decreases
below 96%. This desaturation in highly trained elite athletes likely
614
results from the large right heart cardiac output directed to the lung
during exercise and consequently a decrease in the time the blood
spends in the lung.
Pulmonary Diffusion
Pulmonary diffusion, or gas exchange occurring in the alveoli, is
unaltered at rest and during submaximal exercise following training.
However, it increases at maximal exercise intensity. Pulmonary blood
flow (blood coming from the right side of the heart to the lungs)
increases following training, particularly flow to the upper regions of
the lungs when a person is sitting or standing. This increases lung
perfusion. More blood is brought into the lungs for gas exchange, and
at the same time ventilation increases so that more air is brought into
the lungs. This means that more alveoli will be involved in pulmonary
diffusion. The net result is that pulmonary diffusion increases.
Arterial–Venous Oxygen Difference
It is clear that stroke volume adapts with endurance training, but
peripheral adaptations also contribute to the increase in O2max. The
oxygen content of arterial blood changes very little with endurance
training. Even though total hemoglobin is increased, the amount of
hemoglobin per unit of blood is the same or even slightly reduced.
The (a- )O2 difference, however, does increase with training,
particularly at submaximal exercise intensities. This increase results
from a lower mixed venous oxygen content, reflecting both greater
oxygen extraction by active tissues and a more effective distribution
of blood flow to active tissues. The increased extraction results in part
from an increase in oxidative capacity of active muscle fibers, as
described later in this chapter.
This was demonstrated in a unique longitudinal study involving
both exercise training and a bed-rest deconditioning model.24 Five 20year-old men were tested (baseline values), placed on bed rest for 20
days (deconditioning), and then trained for 60 days, starting
immediately at the conclusion of bed rest. These same five men were
restudied 30 years later at the age of 50; they were tested at baseline
in a relatively sedentary state and after 6 months of endurance
training. The average percentage increases in O2max were similar for
the subjects at age 20 (18%) and at age 50 (14%). However, the
615
increase in O2max at age 20 was explained by increases in both
maximal cardiac output and maximal (a- )O2 difference; at age 50,
the increase was explained primarily by an increase in (a- )O2
difference, while maximal cardiac output was unchanged. Maximal
stroke volume was increased after training at both age 20 and age 50
but to a lesser degree at age 50 (+16 ml/beat at age 20 versus +8
ml/beat at age 50).
While most studies have shown an increase in maximal (a- )O2
difference after aerobic training, a 2015 analysis of the literature
challenged this long-held notion.25 That study reported that, based on
a survey of 13 studies that measured both cardiac output and (a- )O2
difference before and after training, improvements in O2max following
5 to 13 weeks of training were associated with increases in cardiac
output, but not in (a- )O2 difference. That an increase in maximal
cardiac output is the predominant factor associated with increases in
O2max is not surprising, given the close relation between these
variables shown in figure 11.7a. However, the training period in the
studies analyzed was relatively short, so training adaptations may not
have been complete. In longer term endurance training studies,
maximal (a- )O2 differences were enhanced by 1% to 29%25.
In summary, the respiratory system is quite adept at bringing
adequate oxygen into the body. For this reason, the respiratory
system seldom limits endurance performance. Not surprisingly, the
major training adaptations noted in the respiratory system are
apparent mainly during maximal exercise, when all systems are being
maximally stressed.
In Review
Unlike what happens with the cardiovascular system, endurance training has little
effect on lung structure and function.
To support increases in O2max, there is an increase in pulmonary ventilation
during maximal effort following training as both tidal volume and respiratory rate
increase.
Pulmonary diffusion at maximal intensity increases, especially to upper regions of
the lung that are not normally perfused.
Although the largest part of the increase in O2max results from the increases in
cardiac output and muscle blood flow, an increase in (a- O2 difference also plays
616
a key role.
This increase in (a- O2 difference is attributable to a more effective distribution of
arterial blood away from inactive tissue to the active tissue and an increased
ability of active muscle to extract oxygen.
Adaptations in Muscle
Repeated excitation and contraction of muscle fibers during
endurance training stimulate changes in their structure and function.
Our main interest here is in aerobic training and the changes it
produces in muscle fiber type, mitochondrial function, and oxidative
enzymes.
Muscle Fiber Type
As noted in chapter 1, low- to moderate-intensity aerobic activities
rely extensively on type I (slow-twitch) fibers. In response to aerobic
training, type I fibers become larger. More specifically, they develop a
larger cross-sectional area, although the magnitude of change
depends on the intensity and duration of each training bout and the
length of the training program. Increases in cross-sectional area of up
to 25% have been reported. Fast-twitch (type II) fibers, because they
are not being recruited to the same extent during endurance exercise,
generally do not increase cross-sectional area.
Most early studies showed no change in the percentage of type I
versus type II fibers following aerobic training, but subtle changes
were noted among the different type II fiber subtypes. Type IIx fibers
have a low oxidative capacity and are recruited less often than type
IIa fibers during aerobic exercise. However, during long-duration
exercise, these fibers may eventually be recruited to perform in a
manner resembling type IIa fibers. This can cause some type IIx
fibers to take on the characteristics of the more oxidative type IIa
fibers. Recent evidence suggests that not only is there a transition of
type IIx to IIa fibers but also there can be a transition of type II to type
I fibers. The magnitude of change is generally small, not more than a
few percent. As an example, in the HERITAGE Family Study,28 a 20week program of aerobic training increased type I fibers from 43%
pretraining to almost 47% posttraining and decreased type IIx fibers
from 20% to 15%, with type IIa remaining essentially unchanged.
617
These more recent studies have included larger numbers of subjects
and have taken advantage of improved measurement technology;
both might explain why fiber type composition changes within a
muscle are now recognized.
Capillary Supply
One of the most important adaptations to aerobic training is an
increase in the number of capillaries surrounding each muscle fiber.
Table 11.2 illustrates that endurance-trained men have considerably
more capillaries in their leg muscles than sedentary individuals.15
With long periods of aerobic training, the number of capillaries may
increase by more than 15%.28 Having more capillaries allows for
greater exchange of gases, heat, nutrients, and metabolic byproducts between the blood and contracting muscle fibers. In fact, the
increase in capillary density (i.e., increase in capillaries per muscle
fiber) is potentially one of the most important alterations in response
to training that causes the increase in O2max. It is now clear that the
diffusion of oxygen from the capillary to the mitochondria is a major
factor limiting the maximal rate of oxygen consumption by the muscle.
Increasing capillary density facilitates this diffusion, thus maintaining
an environment well suited to energy production and repeated muscle
contractions.
Myoglobin Content
When oxygen enters the muscle fiber, it binds to myoglobin, a
molecule similar to hemoglobin. This iron-containing molecule
shuttles the oxygen molecules from the cell membrane to the
mitochondria. Type I fibers contain large quantities of myoglobin,
which gives these fibers their red appearance (myoglobin is a
pigment that turns red when bound to oxygen). Type II fibers, on the
other hand, are highly glycolytic, so they contain (and require) little
myoglobin—hence their whiter appearance. More important, their
limited myoglobin supply limits their oxidative capacity, resulting in
poor endurance for these fibers.
Myoglobin transports oxygen and releases it to the mitochondria
when oxygen becomes limited during muscle action. This oxygen
reserve is used during the transition from rest to exercise, providing
oxygen to the mitochondria during the lag between the beginning of
618
exercise and the increased cardiovascular delivery of oxygen.
Endurance training has been shown to increase muscle myoglobin
content by 75% to 80%. This adaptation clearly supports a muscle’s
increased capacity for oxidative metabolism after training.
Mitochondrial Function
As noted in chapter 2, oxidative energy production takes place in the
mitochondria. Not surprisingly, aerobic training also induces changes
in mitochondrial function that improve the muscle fibers’ capacity to
produce ATP. The ability to use oxygen and produce ATP via
oxidation depends on the number and size of the muscle
mitochondria. Both increase with aerobic training.
During one study that involved endurance training in rats, the
number of mitochondria increased approximately 15% during 27
weeks of exercise.16 Average mitochondrial size also increased by
about 35% over that training period. As with other training-induced
adaptations, the magnitude of change depends on training volume.
FIGURE 11.9 Endurance exercise training affects the quality of muscle mitochondria by increasing the
production of new, healthy mitochondria (biogenesis), decreasing the degradation of mitochondria, and
clearing away damaged mitochondria (mitophagy). The first two processes are controlled by the
regulator protein PGC-1α. Solid arrows indicate a positive effect while dotted arrows indicate a negative
effect.
Not all mitochondria within a muscle fiber are equally efficient, as
new mitochondria are constantly being formed (biogenesis) and old,
weakened mitochondria are being cleared (mitophagy) (see figure
11.9). Regulation of this mitochondrial turnover cycle determines not
only the number of mitochondria in a fiber but also the overall quantity
and function of those mitochondria,36 which in turn determine overall
metabolic function and performance of skeletal muscles. There has
been an explosion of new research aimed at understanding the
619
underlying molecular mechanisms that regulate mitochondrial
biogenesis, the process by which new mitochondria are formed.
These efforts resulted in the discovery of peroxisome proliferatoractivated receptor-γ coactivator-1α (PGC-1α), a key regulator protein
that is integrally involved in mitochondrial biogenesis in skeletal
muscle. Because of its multiple important roles in enhancing
metabolic function, PGC-1α is often called the master regulator or
master switch. It is also now well established that both acute exercise
and exercise training—both endurance and resistance exercise—
enhance PGC-1α expression.
As shown in figure 11.9, exercise training promotes biogenesis of
new mitochondria, slows the decline in mitochondrial function by
remodeling mitochondria through processes of fusion and fission, and
helps maintain mitophagy in skeletal muscle. Thus, mitochondrial
quality control is an important exercise-induced adaptation.36
Increased expression of PGC-1α protein can be measured in
skeletal muscle even after a single bout of exercise; after two or three
repeated bouts, markers for mitochondrial biogenesis can be
observed. Increased PGC-1α not only increases mitochondrial
biogenesis but also controls the replacement of old weakened
mitochondria with new healthy mitochondria. Mitochondrial damage
induced by such insults as hypoxia, inflammation, or increased
oxidant stress can lead to the accumulation of metabolic by-products
that impair mitochondrial function. Although addition of new
mitochondria is of extreme importance, the maintenance of a healthy
population of mitochondria is equally critical for optimal metabolic
capacity. Continuous removal of damaged mitochondria is likewise
important for optimal function of skeletal muscle.
Oxidative Enzymes
Regular endurance exercise has been shown to induce major
adaptations in skeletal muscle, including an increase in the number
and size of the muscle fiber mitochondria as just discussed. These
changes are further enhanced by an increase in mitochondrial
capacity. The oxidative breakdown of fuels and the ultimate
production of ATP depend on the action of mitochondrial oxidative
enzymes, the specialized proteins that catalyze (i.e., speed up) the
620
breakdown of nutrients to form ATP. Aerobic training increases the
activity of these important enzymes.
Figure 11.10 illustrates the changes in the activity of succinate
dehydrogenase (SDH), a key muscle oxidative enzyme, over 7
months of progressive swim training. While the rate of increases in
O2max slowed after the first 2 months of training, activity of this key
oxidative enzyme continued to increase throughout the entire training
period. This suggests that training-induced increases in O2max might
be limited more by the circulatory system’s ability to transport oxygen
than by the muscles’ oxidative potential.
FIGURE 11.10 The percentage change in maximal oxygen uptake ( O2max) and the activity of
succinate dehydrogenase (SDH), one of the muscles’ key oxidative enzymes, during 7 months of swim
training. Interestingly, although this enzyme activity continues to increase with increasing levels of
621
training, the swimmers’ maximal oxygen uptake appears to level off after the first 8 to 10 weeks of
training. This implies that mitochondrial enzyme activity is not a direct indication of whole-body
endurance capacity.
The activities of muscle enzymes such as SDH and citrate
synthase are dramatically influenced by aerobic training. This is seen
in figure 11.11, which compares the activities of these enzymes in
untrained people, moderately trained joggers, and highly trained
runners.9 Even moderate daily exercise increases the activity of these
enzymes and thus the oxidative capacity of the muscle. For example,
jogging or cycling for as little as 20 min per day has been shown to
increase SDH activity in leg muscles by more than 25%. Training
more vigorously—for example, for 60 to 90 min per day—produces a
two- to threefold increase in this enzyme’s activity.
One metabolic consequence of mitochondrial changes induced by
aerobic training is glycogen sparing, a slower rate of utilization of
muscle glycogen and enhanced reliance on fat as a fuel source at a
given exercise intensity. Enhanced glycogen sparing with endurance
training most likely improves the ability to sustain a higher exercise
intensity, such as maintaining a faster race pace in a 10 km run.
622
FIGURE 11.11 Leg muscle (gastrocnemius) enzyme activities of untrained (UT) subjects, moderately
trained (MT) joggers, and highly trained (HT) marathon runners. Enzyme levels are shown for two of
many key enzymes that participate in the oxidative production of adenosine triphosphate.
Adapted from Costill, Fink, Lesmes, et al. (1979); Costill, Coyle, Fink, et al. (1979).
In summary, endurance exercise training causes a wide variety of
phenotypic adaptations in skeletal muscle, including angiogenesis
(creation of new capillaries), transformation of fiber types from
glycolytic to oxidative, increased ability to mobilize and use fats as a
substrate, and increased glucose uptake by muscle fibers, which
increases the number of mitochondria and improves the overall
quality of the existing mitochondrial pool.
In Review
623
Aerobic training selectively recruits type I muscle fibers and fewer type II fibers.
Consequently, the type I fibers increase their cross-sectional area with aerobic
training.
After training, there appears to be a small increase in the percentage of type I
fibers, as well as a transition of some type IIx to type IIa fibers.
Aerobic training increases both the number of capillaries per muscle fiber and the
number of capillaries for a given cross-sectional area of muscle. These changes
improve blood perfusion through the muscles, enhancing the diffusion of oxygen,
carbon dioxide, nutrients, and by-products of metabolism between the blood and
muscle fibers.
Aerobic training increases muscle myoglobin content by as much as 80%.
Myoglobin transports oxygen from cell membranes to the mitochondria.
Aerobic training increases both the number and the size of muscle fiber
mitochondria, providing the muscle with an increased capacity for oxidative
metabolism.
Endurance exercise training also improves the overall quality of the existing
mitochondrial pool.
Activities of many oxidative enzymes are increased with aerobic training.
These changes occurring in the muscles, combined with adaptations in the
oxygen transport system, enhance the capacity of oxidative metabolism and
improve endurance performance.
Metabolic Adaptations to Training
Now that we have discussed training changes in both the
cardiovascular and respiratory systems, as well as skeletal muscle
adaptations, we are ready to examine how these integrated
adaptations are reflected by changes in three important physiological
variables related to metabolism:
Lactate threshold
Respiratory exchange ratio
Oxygen consumption
Lactate Threshold
Lactate threshold, discussed in chapter 5, is a physiological marker
that is closely associated with endurance performance—the higher
the lactate threshold, the better the performance capacity. Figure
624
11.12a illustrates the difference in lactate threshold between an
endurance-trained individual and an untrained individual. This figure
also accurately represents the changes in lactate threshold that
would occur following a 6- to 12-month program of endurance
training. In either case, in the trained state, one can exercise at a
higher percentage of one’s
O2max before lactate begins to
accumulate in the blood. In this example, the trained runner could
sustain a race pace of 70% to 75% of O2max, an intensity that would
result in continued lactate accumulation in the blood of the untrained
runner. This translates into a much faster race pace (see figure
11.12b). Above the lactate threshold, the lower lactate at a given rate
of work is likely attributable to a combination of reduced lactate
production and increased lactate clearance. As athletes become
better trained, their postexercise blood lactate concentrations are
lower for a given rate of work.
Respiratory Exchange Ratio
Recall from chapter 5 that the respiratory exchange ratio (RER) is the
ratio of carbon dioxide released to oxygen consumed during
metabolism. The RER reflects the composition of the mixture of
substrates being used as an energy source, with a lower RER
reflecting an increased reliance on fats for energy production and a
higher RER reflecting a higher contribution of carbohydrates.
After training, the RER decreases at both absolute and relative
submaximal exercise intensities. These changes are attributable to a
greater utilization of free fatty acids instead of carbohydrate at these
work rates following training.
Resting and Submaximal Oxygen Consumption
Oxygen consumption ( O2) at rest is unchanged following endurance
training. While a few cross-sectional comparisons have suggested
that training elevates resting O2, the HERITAGE Family Study—with
a large number of subjects and with duplicate measures of resting
metabolic rate both before and after 20 weeks of training—showed no
evidence of an increased resting metabolic rate after training.35
During submaximal exercise at a given intensity, O2 is either
unchanged or slightly reduced following training. In the HERITAGE
625
Family Study, training reduced submaximal O2 by 3.5% at a work
rate of 50 W. There was a corresponding reduction in cardiac output
at 50 W, reinforcing the strong interrelationship between O2 and
cardiac output.34 This small decrease in O2 during submaximal
exercise, not seen in many studies, could have resulted from an
increase in exercise economy (performing the same exercise
intensity with less extraneous movement).
FIGURE 11.12 Changes in lactate threshold (LT) with training expressed as (a) a percentage of
maximal oxygen uptake (% O2max) and (b) an increase in speed on the treadmill. Lactate threshold
occurs at a speed of 8.4 km/h (5.2 mph) in the untrained state and at 11.6 km/h (7.2 mph) in the trained
state.
Maximal Oxygen Consumption
O2max is the best indicator of cardiorespiratory endurance capacity
and increases substantially in response to endurance training. While
small and very large increases have been reported, an increase of
15% to 20% is typical for a previously sedentary person who trains at
50% to 85% of his or her O2max three to five times per week, 20 to
60 min per day, for 6 months. For example, the O2max of a sedentary
individual could reasonably increase from 35 ml · kg−1 · min−1 to 42 ml
· kg−1 · min−1 as a result of such a program. This is far below the
values we see in world-class endurance athletes, whose values
generally range from 70 to 94 ml · kg−1 · min−1. The more sedentary
an individual is when starting an exercise program, the larger the
increase in O2max.
Integrated Adaptations to Chronic Endurance Exercise
626
It should now be clear that the adaptations that accompany
endurance training are many and that they affect multiple
physiological systems. Physiologists commonly establish models to
help explain how various physiological factors or variables work
together to affect a specific outcome or component of performance.
Dr. Donna H. Korzick, an exercise physiologist at Pennsylvania State
University, has created a unifying figure to model the factors that
contribute to the cardiovascular adaptation to chronic endurance
training (see figure 11.13).
What Limits Aerobic Power and Endurance Performance?
A number of years ago, exercise scientists were divided on what
major physiological factor or factors actually limit
O2max. Two
contrasting theories had been proposed.
FIGURE 11.13 Cardiovascular adaptations to chronic endurance exercise.
Adapted by permission from Donna H. Korzick, Pennsylvania State University, 2006.
One theory held that endurance performance was limited by the
lack of sufficient concentrations of oxidative enzymes in the
mitochondria. Endurance training programs substantially increase
these oxidative enzymes, allowing active tissue to use more of the
available oxygen, resulting in a higher O2max. In addition, endurance
training increases both the size and number of muscle mitochondria.
627
Thus, this theory argued, the main limitation of maximal oxygen
consumption is the inability of the existing mitochondria to use the
available oxygen beyond a certain rate. This theory was referred to
as the utilization theory.
The second theory proposed that central and peripheral
cardiovascular factors limit endurance capacity. These circulatory
influences would preclude delivery of sufficient amounts of oxygen to
the active tissues. Taking into account the observation that
improvement in O2max following endurance training results from
increased blood volume, increased cardiac output (via stroke
volume), and a better perfusion of active muscle with blood, this
theory proposed that these cardiovascular factors are the limiting
factor for O2max.
Evidence strongly supports the latter theory. In one study, subjects
breathed a mixture of carbon monoxide (which irreversibly binds to
hemoglobin, limiting hemoglobin’s oxygen-carrying capacity) and air
during exercise to exhaustion.26
O2max decreased in direct
proportion to the percentage of carbon monoxide breathed. The
carbon monoxide molecules bonded to approximately 15% of the
total hemoglobin; this percentage agreed with the percentage
reduction in O2max. In another study, approximately 15% to 20% of
each subject’s total blood volume was removed.11 O2max decreased
by approximately the same relative amount. Reinfusion of the
subjects’ packed red blood cells approximately 4 weeks later
increased O2maxwell above baseline or control conditions. In both
studies, the reduction in the oxygen-carrying capacity of the blood—
via either blocking hemoglobin or removing whole blood—resulted in
the delivery of less oxygen to the active tissues and a corresponding
reduction in O2max. Similarly, studies have shown that breathing
oxygen-enriched mixtures, in which the partial pressure of oxygen in
the inspired air is substantially increased, increases endurance
capacity.
These and subsequent studies indicated that the available oxygen
supply is the major limiter of endurance performance. Oxygen
transport to the working muscles, not the available mitochondria and
oxidative enzymes, limits O2max. The argument was that increases in
628
O2max with training are largely attributable to increased maximal
blood flow and increased muscle capillary density in the active
tissues. Skeletal muscle adaptations (including increased
mitochondrial content and respiratory capacity of the muscle fibers)
contribute importantly to the ability to perform prolonged, highintensity, submaximal exercise.
Table 11.3 summarizes the typical physiological changes that
occur with endurance training. The values (pre- and posttraining) for
a previously inactive man are compared with values for a world-class
male endurance runner.
In Review
Lactate threshold increases with endurance training, allowing performance of
higher exercise intensities without significantly increasing blood lactate
concentration.
With endurance training, the RER decreases at submaximal work rates, indicating
greater utilization of free fatty acids as an energy substrate (carbohydrate
sparing).
Oxygen consumption generally remains unchanged at rest and remains unaltered
or decreases slightly during submaximal exercise following endurance training.
O2max increases substantially following endurance training, but the extent of
increase possible is genetically limited in each individual. The major limiting factor
appears to be oxygen delivery to the active muscles.
Long-Term Improvement in Aerobic Power and
Cardiorespiratory Endurance
Although an individual’s highest attainable O2max is usually achieved
within 12 to 18 months of intense endurance training, endurance
performance can continue to improve. Improvement in endurance
performance without improvement in O2max is likely attributable to
improvements in the ability to perform at increasingly higher
percentages of O2max for extended periods. Consider, for example, a
young male runner who starts training with an initial O2max of 52.0 ml
· kg−1 · min−1. He reaches his genetically determined peak O2max of
71.0 ml · kg−1 · min−1 after 2 years of intense training, after which no
further increases occur, even with more frequent or more intense
629
workouts. At this point, as shown in figure 11.14, the young runner is
able to run at 75% of his O2max (0.75 × 71.0 = 53.3 ml · kg−1 · min−1)
in a 10 km (6.2 mi) race. After an additional 2 years of intensive
training, his O2max is unchanged, but he is now able to compete at
88% of his O2max (0.88 × 71.0 = 62.5 ml · kg−1 · min−1). Obviously, by
being able to sustain an oxygen uptake of 62.5 ml · kg−1 · min−1, he is
able to run at a much faster race pace.
This ability to sustain exercise at a higher percentage of O2max is
partly the result of an increase in the ability to buffer lactate, because
race pace is directly related to the O2 value at which lactate begins
to accumulate.
TABLE 11.3 Typical Effects of Endurance Training in a
Previously Inactive Man, Contrasted with Values for a Male
World-Class Endurance Athlete
Variables
Pretraining, sedentary
male
Posttraining, sedentary
male
World-class endurance
athlete
Cardiovascular
HRrest (beats/min)
75
65
45
HRmax (beats/min)
185
183
174
SVrest (ml/beat)
60
70
100
SVmax (ml/beat)
120
140
200
at rest (L/min)
max (L/min)
Heart volume (ml)
Blood volume (L)
Systolic BP at rest (mmHg)
Systolic BPmax (mmHg)
Diastolic BP at rest (mmHg)
Diastolic BPmax (mmHg)
4.5
22.2
4.5
25.6
4.5
34.8
750
4.7
135
200
820
5.1
130
210
1,200
6.0
120
220
78
82
76
80
65
65
Respiratory
E
at rest (L/min)
(L/min)
TV at rest (L)
TVmax (L)
VC (L)
RV (L)
7
6
6
110
135
195
0.5
2.75
0.5
3.00
0.5
3.90
5.8
1.4
6.0
1.2
6.2
1.2
E max
Metabolic
(a- O2 diff at rest (ml/100 ml)
(a- O2 diff max (ml/100 ml)
O2 at rest (ml · kg−1 ·
min−1)
O2max (ml · kg−1 · min−1)
Blood lactate at rest (mmol/L)
Blood lactate max (mmol/L)
6.0
6.0
6.0
14.5
15.0
16.0
3.5
3.5
3.5
40.7
49.9
81.9
1
7.5
1
8.5
1
9.0
630
Body composition
Weight (kg)
Fat weight (kg)
Fat-free weight (kg)
Fat (%)
79
12.6
66.4
16.0
Note. HR = heart rate; SV = stroke volume;
77
9.6
67.4
12.5
= cardiac output; BP = blood pressure;
68
5.1
62.9
7.5
E
vital capacity; RV = residual volume; (a- O2 diff = arterial–mixed venous oxygen difference;
= ventilation; TV = tidal volume; VC =
O2 = oxygen consumption.
Factors Affecting an Individual’s Response to Aerobic Training
We have discussed general trends in adaptations that occur in
response to endurance training. However, we must always remember
that we are talking about adaptations in individuals and that everyone
does not respond in the same manner. Several factors that can affect
individual response to aerobic training must be considered.
Training Status and O2max
The higher the initial state of conditioning, the smaller the relative
improvement for the same volume of training. For example, if two
people, one sedentary and the other partially trained, undergo the
same endurance training program, the sedentary person will show
the greatest relative (%) improvement.
631
FIGURE 11.14 Change in race pace with continued training after maximal oxygen uptake stops
increasing beyond 71 ml · kg−1 · min−1.
In fully mature athletes, the highest attainable O2max is reached
within 8 to 18 months of intense endurance training, indicating that
each athlete has a finite maximal attainable level of oxygen
consumption. This finite range is genetically determined but may
potentially be influenced by training in early childhood during the
development of the cardiovascular system.
Heredity
The ability to increase maximal oxygen consumption levels is
genetically limited. This does not mean that each individual has a
preprogrammed O2max that cannot be exceeded. Rather, a range of
O2maxvalues seems to be predetermined by an individual’s genetic
makeup, with that individual’s highest attainable O2max somewhere
in that range. Each individual is born into a predetermined genetic
window, and the person can shift up or down within that window with
exercise training or detraining, respectively.
632
Research on the genetic basis of O2max began in the late 1960s
and early 1970s. Recent research has shown that identical
(monozygous) twins have similar
O2max values, whereas the
variability for dizygous (fraternal) twins is much greater (see figure
11.15).5 Each symbol represents a pair of brothers. Brother A’s
O2max value is indicated by the symbol’s position on the x-axis, and
brother B’s O2max value is on the y-axis. Similarity in the siblings’
O2max values is noted by comparing the x and y coordinates of the
symbol (i.e., how close it falls to the diagonal line x = y on the graph).
Similar results were found for endurance capacity, determined by the
maximal amount of work performed in an all-out, 90 min ride on a
cycle ergometer.
633
FIGURE 11.15 Comparisons of
O2max in twin (monozygous and dizygous) and nontwin brothers.
Adapted by permission from C. Bouchard et al., “Aerobic Performance in Brothers, Dizygotic and Monozygotic
Twins,” Medicine and Science in Sports and Exercise 18 (1986): 639-646.
Bouchard and colleagues4 concluded that heredity accounts for
between 25% and 50% of the variance in O2maxx values. This means
that of all factors influencing O2max, heredity alone is responsible for
one-quarter to one-half of the total influence. World-class athletes
who have stopped endurance training continue for many years to
have high O2max values in their sedentary, deconditioned state. Their
O2max values may decrease from 85 to 65 ml · kg−1 · min−1, but this
deconditioned value is still very high compared with that of the
general population.
Heredity also potentially explains the fact that some people have
relatively high
O2max values yet have no history of endurance
training. In a study that compared untrained men who had O2max
values below 49 ml · kg−1 · min−1 with untrained men who had O2max
values above 62.5 ml · kg−1 · min−1, those with high values were
distinguished by having higher blood volumes, which contributed to
higher stroke volumes and cardiac outputs at maximal intensities.
The higher blood volumes in the high O2max group were most likely
genetically determined.11
Thus, both genetic and environmental factors influence O2max
values. The genetic factors probably establish the boundaries for the
athlete, but endurance training can push O2max to the upper limit of
these boundaries. Dr. Per-Olof Åstrand, one of the most highly
recognized exercise physiologists during the second half of the 20th
century, stated on numerous occasions that the best way to become
a champion Olympic athlete is to be selective when choosing one’s
parents!
Sex
634
Healthy untrained girls and women have significantly lower O2max
values (20%-25% lower) than healthy untrained boys and men.
Highly conditioned female endurance athletes have values much
closer to those of highly trained male endurance athletes (i.e., only
about 10% lower). This is discussed in greater detail in chapter 19.
Representative ranges of O2max values for athletes and nonathletes
are presented in table 11.4 by age, sex, and sport.
High Responders and Low Responders
For years, researchers have found wide variations in the amount of
improvement in
O2max with endurance training. Studies have
demonstrated individual improvements in O2max ranging from 0% to
50% or more, even in similarly fit subjects completing exactly the
same training program.
TABLE 11.4 Maximal Oxygen Uptake Values (ml · kg−1 · min−1)
for Nonathletes and Athletes
Group or sport
Age group (years)
Males
Females
Nonathletes
10-19
20-29
30-39
40-49
50-59
60-69
70-79
18-32
18-30
18-26
22-28
20-36
18-22
10-30
20-40
20-60
20-35
20-35
18-30
20-28
18-24
22-28
18-24
10-25
22-30
18-39
40-75
22-30
18-22
20-30
20-30
47-56
43-52
39-48
36-44
34-41
31-38
28-35
48-56
40-60
62-74
55-67
42-60
52-58
50-63
50-60
47-53
55-62
60-72
57-68
65-94
58-63
54-64
56-73
50-70
42-55
60-85
40-60
40-46
38-46
33-42
30-38
26-35
24-33
22-30
20-27
52-57
43-60
47-57
48-52
Baseball and softball
Basketball
Bicycling
Canoeing
Football
Gymnastics
Ice hockey
Jockey
Orienteering
Racquetball
Rowing
Skiing, alpine
Skiing, Nordic
Ski jumping
Soccer
Speed skating
Swimming
Track and field, discus
Track and field, running
Track and field, shot put
Volleyball
Weightlifting
Wrestling
38-52
52-65
36-50
46-60
50-60
58-65
50-55
60-75
50-60
44-55
40-60
*
50-75
35-60
*
40-56
*
*Data not available.
In the past, exercise physiologists have assumed that these
variations result from differing degrees of compliance with the training
635
program. People who comply with the program should, and do, have
the highest percentage of improvement, and poor compliers should
show little or no improvement. However, given the same training
stimulus and full compliance with the program, substantial variations
still occur in the percent improvement in O2max for different people.
It is now evident that some of the response to a training program is
also genetically determined. This is illustrated in figure 11.16. Ten
pairs of identical twins completed a 20-week endurance training
program; the improvements in O2max, expressed as percentages,
are plotted for each twin pair—twin A on the x-axis and twin B on the
y-axis.27 Notice the similarity in response of each twin pair. Yet across
twin pairs, improvement in O2max varied from 0% to 40%. These
results, and those from other studies, indicate that there will be high
responders (showing large improvement) and low responders
(showing little or no improvement) among groups of people who
participate in identical training programs. However, while genetic
variants may be involved, such variants appear to be associated with
the physiological mechanisms (increased cardiac output, expanded
blood volume, improved muscle oxygen extraction) that underpin
such differences.20
Results from the HERITAGE Family Study also support a strong
genetic component in the magnitude of increase in O2max with
endurance training. Families, including the biological mother and
father and three or more of their children, trained 3 days a week for
20 weeks, initially exercising at a heart rate equal to 55% of their
O2max for 35 min per day and progressing to a heart rate equal to 75%
of their O2max for 50 min per day by the end of the 14th week, which
they maintained for the last 6 weeks.3 The average increase in
O2max was about 17% but varied from 0% to more than 50%. Figure
11.17 illustrates the improvement in O2max for each subject in each
family. Maximal heritability was estimated at 47%. Note that subjects
who are high responders tend to be clustered in the same families, as
are those who are low responders.
636
FIGURE 11.16 Variations in the percentage increase in
same 20-week training program.
O2max for identical twins undergoing the
Reprinted by permission from D. Prud’homme et al., “Sensitivity of Maximal Aerobic Power to Training is GenotypeDependent,” Medicine and Science in Sports and Exercise 16, no. 5 (1984): 489-493.
It is clear that this is a genetic phenomenon, not a result of
compliance or noncompliance. One must consider this important
point when conducting training studies and designing training
programs. Individual differences must always be accounted for.
Cardiorespiratory Endurance in Nonendurance Sports
Many people regard cardiorespiratory endurance as the most
important component of physical fitness. Low endurance capacity
leads to fatigue, even in activities that are not aerobic. For any
athlete, regardless of the sport or activity, fatigue represents a major
deterrent to optimal performance. Even minor fatigue can hinder the
athlete’s total performance:
Muscular strength is decreased.
Reaction and movement times are prolonged.
Agility and neuromuscular coordination are reduced.
637
Whole-body movement speed is slowed.
Concentration and alertness are reduced.
The decline in concentration and alertness associated with fatigue
is particularly important. The athlete can become careless and more
prone to serious injury, especially in contact sports. Even though
these decrements in performance might be small, they can be just
enough to cause an athlete to miss the critical free throw in
basketball, the strike zone in baseball, or the 20 ft (6 m) putt in golf.
All athletes can benefit from improving their cardiorespiratory
endurance. Even golfers, whose sport demands little in the way of
aerobic endurance, can benefit. Improved endurance can allow
golfers to complete a round of golf with less fatigue and to better
withstand long periods of walking and standing.
For the sedentary, middle-aged adult, numerous health factors
indicate that cardiovascular endurance should be the primary
emphasis of training. Training for health and fitness is discussed at
length in part VII of this book.
FIGURE 11.17 Variations in the improvement in
O2max following 20 weeks of endurance training by
families. Values represent the changes in O2max in ml/min, with an average increase of 393 ml/min.
Data for each family are enclosed within a bar, and each family member’s value is represented as a dot
within the bar.
Adapted by permission from C. Bouchard, P. An, T. Rice, J.S. Skinner, J.H. Wilmore et al., “Familial Aggregation of
O2max Response to Exercise Training. Results from HERITAGE Family Study,” Journal of Applied Physiology 87
(1999): 1003-1008.
638
The extent of endurance training needed varies considerably from
one sport to the next and from one athlete to the next. It depends on
the athlete’s current endurance capacity and the endurance demands
of the chosen activity. However, adequate cardiovascular conditioning
must be the foundation of any athlete’s general conditioning program.
In Review
Although improvements in O2max eventually plateau, endurance performance
can continue to improve for years with continued training.
An individual’s genetic makeup predetermines a range for that person’s
and accounts for 25% to 50% of the variance in O2max values.
O2max
Heredity also largely explains individual variations in response to identical training
programs.
Highly conditioned female endurance athletes have O2max values only about
10% lower than those of highly conditioned male endurance athletes.
All athletes, regardless of their sport or event, can benefit from maximizing their
cardiorespiratory endurance.
Aerobic Deconditioning
Issues related to deconditioning are particularly relevant to bed rest
associated with diseases and disability as well as to the space
program, since weightlessness and bed rest cause similar declines in
O2max. According to a recent analysis, 80 studies with a total of 949
participants have been published since 1949 that reported the effects
of total bed rest on O2max.29 The studies were conducted mainly in
young (age range 22-34 years), male (>90%) subjects with bed rest
lasting from 1 to 90 days. Declines in O2max were fairly linear
throughout periods of prolonged bed rest.
Surprisingly, while body weight and lean body mass both decline in
response to bed rest, those changes were unrelated to the decline in
O2max. The most important predictor of how much O2max dropped
was the subjects’ fitness level at the beginning of the bed rest period.
Higher initial O2max levels were associated with larger declines in
O2max.
Adaptations to Anaerobic Training
639
In muscular activities that require near-maximal force production for
relatively short periods of time, such as sprinting, much of the energy
needs are met by the ATP-phosphocreatine (PCr) system and the
anaerobic breakdown of muscle glycogen (glycolysis). The following
sections focus on the trainability of these two systems.
Changes in Anaerobic Power and Anaerobic Capacity
Exercise scientists have had difficulty agreeing on an appropriate
laboratory or field test to measure anaerobic power. Unlike the
situation with aerobic power, for which O2max is generally agreed to
be the gold standard measurement, no single test adequately
measures anaerobic power. Most research has been conducted
through use of three different tests of either anaerobic power,
anaerobic capacity, or both: the Wingate anaerobic test, the critical
power test, and the maximal accumulated oxygen deficit test. Of
these three, the Wingate test has been the most widely used. Despite
the limitations inherent in each of these methods, they remain our
only indirect indicators of the metabolic potential of anaerobic
capacity.
640
As described in chapter 9, the Wingate anaerobic test is commonly
used to measure anaerobic power. Peak power output, the highest
mechanical power achieved during the first 5 to 10 s, is considered
an index of anaerobic power. The mean power output is computed as
the average power output over the total 30 s period, and one obtains
total work simply by multiplying the mean power output by 30 s. Mean
power output and total work have both been used as indexes of
anaerobic capacity.
With anaerobic training, such as sprint training on the track or on a
cycle ergometer, there are increases in both peak anaerobic power
and anaerobic capacity. However, results have varied widely across
641
studies, from those that showed only minimal increases to those
showing increases of up to 25%.
Adaptations in Muscle with Anaerobic Training
With anaerobic training, which includes sprint training and resistance
training, there are changes in skeletal muscle that specifically reflect
muscle fiber recruitment for these types of activities. As discussed in
chapter 1, at higher intensities, type II muscle fibers are recruited to a
greater extent, but not exclusively, because type I fibers continue to
be recruited. Overall, sprint and resistance activities use the type II
muscle fibers significantly more than do aerobic activities.
Consequently, both type IIa and type IIx muscle fibers undergo an
increase in their cross-sectional areas. The cross-sectional area of
type I fibers also is increased but usually to a lesser extent.
Furthermore, with sprint training there appears to be a reduction in
the percentage of type I fibers and an increase in the percentage of
type II fibers, with the greatest change in type IIa fibers. In two of
these studies, in which subjects performed 15 to 30 s all-out sprints,
the type I percentage decreased from 57% to 48% and type IIa
increased from 32% to 38%.17,18 This shift of type I to type II fibers is
not typically seen with resistance training.
Adaptations in the Energy Systems
Just as aerobic training produces changes in the aerobic energy
system, anaerobic training alters the ATP-PCr and anaerobic
glycolytic energy systems. These changes are not as obvious or
predictable as those that result from endurance training, but they do
improve performance in anaerobic activities.
Adaptations in the ATP-PCr System
Activities that emphasize maximal muscle force production, such as
sprinting and weightlifting events, rely most heavily on the ATP-PCr
system for energy. Maximal effort lasting less than about 6 s places
the greatest demands on the breakdown and resynthesis of ATP and
PCr. Costill and coworkers reported their findings from a study of
resistance training and its effects on the ATP-PCr system.8 Their
participants trained by performing maximal knee extensions. One leg
was trained using 6 s maximal work bouts that were repeated 10
642
times. This type of training preferentially stressed the ATP-PCr
energy system. The other leg was trained with repeated 30 s maximal
bouts, which instead preferentially stressed the glycolytic system.
The two forms of training produced the same muscular strength
gains (about 14%) and the same resistance to fatigue. As seen in
figure 11.18, the activities of the anaerobic muscle enzymes creatine
kinase and myokinase increased as a result of the 30 s training bouts
but were almost unchanged in the leg trained with repeated 6 s
maximal efforts. This finding leads us to conclude that maximal sprint
bouts (6 s) might improve muscular strength but contribute little to the
mechanisms responsible for ATP and PCr breakdown. Data have
been published, however, that show improvements in ATP-PCr
enzyme activities with training bouts lasting only 5 s.
Regardless of the conflicting results, these studies suggest that the
major value of training bouts that last only a few seconds (sprints) is
the development of muscular strength. Such strength gains enable
the individual to perform a given task with less effort, which reduces
the risk of fatigue. Whether these changes allow the muscle to
perform more anaerobic work remains unanswered, although a 60 s
sprint-fatigue test suggests that short sprint-type anaerobic training
does not enhance anaerobic endurance.8
FIGURE 11.18 Changes in creatine kinase (CK) and muscle myokinase (MK) activities as a result of 6
s and 30 s bouts of maximal anaerobic training.
643
Adaptations in the Glycolytic System
Anaerobic training (30 s bouts) increases the activities of several key
glycolytic enzymes. The most frequently studied glycolytic enzymes
are phosphorylase, phosphofructokinase (PFK), and lactate
dehydrogenase (LDH). The activities of these three enzymes
increased 10% to 25% with repeated 30 s training bouts but changed
little with short (6 s) bouts that stress primarily the ATP-PCr system.8
In another study, 30 s maximal all-out sprints significantly increased
hexokinase (56%) and PFK (49%) but not total phosphorylase activity
or LDH.21
Because both PFK and phosphorylase are essential to the
anaerobic yield of ATP, such training might enhance glycolytic
capacity and allow the muscle to develop greater tension for a longer
period of time. However, as seen in figure 11.19, this conclusion is not
supported by results of a 60 s sprint performance test, in which the
subjects performed maximal knee extension and flexion. Power
output and the rate of fatigue (shown by a decrease in power
production) were affected to the same degree after sprint training with
either 6 s or 30 s training bouts. Thus, we must conclude that
performance gains with these forms of training result from
improvements in strength rather than improvements in the anaerobic
yield of ATP.
644
FIGURE 11.19 Performance in a 60 s sprint bout after training with 6 s and 30 s anaerobic bouts.
Subjects are the same as in figure 11.18.
Adaptations to High-Intensity Interval Training
In chapter 9 we introduced a special form of training using short
bursts of very intense cycling, interspersed with up to a few minutes
of rest or low-intensity cycling for recovery.14 High-intensity interval
training (HIIT) is a time-efficient way to induce many aerobic training
benefits normally associated with continuous running, cycling, or
swimming.
Adaptations to HIIT mirror those associated with more traditional
aerobic training. In one study, untrained young subjects performed
four to six 30 s sprints separated by 4 min of recovery, three times a
week. These men showed the same beneficial changes in their heart,
blood vessels, and muscles as another group who underwent a
traditional training program involving up to an hour of continuous
cycling, 5 days per week. Improvements in exercise performance—
whether measured as cycling time to exhaustion at a fixed work
intensity or in time trials that more closely resemble normal athletic
competition—were
comparable
between
groups,
despite
considerable differences in training time commitment.14 High-intensity
interval training appears to stimulate some of the same molecular
signaling pathways that regulate skeletal muscle remodeling in
response to endurance training, including mitochondrial biogenesis
and changes in the capacity for carbohydrate and fat transport and
oxidation.
In Review
Anaerobic training bouts improve both anaerobic power and anaerobic capacity.
The performance improvement noted with sprint-type anaerobic training appears
to result more from strength gains than from improvements in the functioning of
the anaerobic energy systems.
Anaerobic training increases the ATP-PCr and glycolytic enzymes but has no
effect on the oxidative enzymes.
Conversely, aerobic training increases the oxidative enzymes but has little effect
on the ATP-PCr or glycolytic enzymes.
645
Adaptations to HIIT mirror those associated with more traditional aerobic training.
High-intensity interval training appears to stimulate some of the same molecular
signaling pathways that regulate skeletal muscle remodeling in response to
endurance training, including mitochondrial biogenesis and changes in the
capacity for carbohydrate and fat transport and oxidation.
RESEARCH PERSPECTIVE 11.2
Brief, Intense Stair Climbing
Low cardiorespiratory fitness is a strong predictor of cardiovascular disease
and death. Public health guidelines generally recommend 150 min/week of
moderate-intensity physical activity to achieve health benefits, but less than
15% of North Americans meet that recommendation. Lack of time and lack of
necessary equipment are the two most commonly cited reasons for not
achieving the recommended daily physical activity. Because of this, public
health researchers and exercise physiologists are interested in finding easily
accessible and briefer exercise protocols that achieve the same health
benefits as the current 150 min/week of moderate-intensity exercise
recommendation.
High-intensity interval training, or HIIT, which involves brief intermittent
bursts of high-intensity exercise separated by recovery periods, improves
cardiorespiratory fitness. Sprint interval training has been shown to improve
fitness and insulin sensitivity to the same extent as a moderate-intensity
continuous exercise protocol that required five times as much time to
complete. Knowing this, a research team at McMaster University in Canada
recently conducted a series of studies to see if brief, intense stair climbing, a
readily available high-intensity activity, could improve cardiorespiratory
fitness.1 In these studies, young, sedentary women performed an acute
exercise comparison to ensure that the stair-climbing protocol elicited the
same acute physiological responses as a classical sprint interval training bout
on a stationary bike, and a 6-week training intervention. In the intervention
period, subjects were instructed to perform three 20 s bursts of all-out intensity
going up the stairs as fast as possible with 2 min of recovery between bouts, 3
days/week.
Work output, heart rate, blood lactate, and RPE responses were the same
between the brief intense stair-climbing protocol and the classical sprint
interval training protocol. Following 6 weeks of stair-climbing training,
cardiorespiratory fitness ( O2peak) had improved by 12%, which is similar to
other studies using a cycle ergometer to administer sprint interval training.
Importantly, the study team also reported that the participants completed 99%
of all the training sessions and that the average time required to complete the
training was ≤9 min/week. Overall, brief, intense stair climbing is a time-
646
efficient and easily accessible mode of exercise that can increase
cardiorespiratory fitness in sedentary adults.
RESEARCH PERSPECTIVE 11.3
Do Ice Baths Increase Recovery and Endurance
Performance?
Postexercise cold-water immersion has become increasingly popular in
athletic training programs because of the belief that it speeds up recovery.
However, few studies have scientifically investigated the effect of postexercise
cold-water immersion therapy on the adaptive responses to endurance
training, and no studies have examined these effects with sprint interval
training. Of the research studies that have been conducted, the results have
been conflicting. Some suggest that cold-water immersion may stimulate
muscle mitochondria biogenesis and allow for better recovery and harder
training in subsequent bouts of exercise, while other say that postexercise
cold-water immersion may counteract the molecular processes related to
vascular remodeling and have detrimental long-term effects on skeletal
muscle adaptations to endurance training. Overall, the utility of postexercise
cold-water immersion to enhance recovery and subsequent performance is
still unclear.
A recent study conducted at Victoria University in Australia investigated the
effects of cold-water immersion on mitochondrial content and function within
the muscle (1) following a single bout of sprint interval (HIIT) exercise and (2)
after a 6-week HIIT intervention.7 The researchers recruited healthy,
recreationally active men and split them into two groups. One group received
postexercise cold-water immersion after each training bout, while the other
group performed the same training but had a passive recovery without cold
water. After a baseline familiarization trial, subjects performed a single bout of
HIIT training followed by a skeletal muscle biopsy. After the 6-week training
intervention, another muscle biopsy was done along with posttraining time-trial
and O2max testing. The investigators analyzed the skeletal muscle biopsies
for p-AMPK, p-p38 MAPK, p-p53, and PGC-1α, which are markers of
mitochondrial content and function. In short, the investigators did not find any
effect of cold-water immersion on any of their measurements. There were no
differences between the group of participants who were treated with coldwater immersion after each exercise bout and the control group, who
performed the exercise training without cold-water immersion during recovery.
This program of HIIT increased O2max and time trial performance without any
effect on markers of mitochondrial content or function.
While these findings suggest that cold-water immersion is not detrimental
to endurance adaptations after sprint interval training, they also suggest that
647
cold-water immersion does not provide any benefit to endurance training
adaptations or improvements in fitness and performance.
As discussed in chapter 9, athletes who already train vigorously
can likewise improve performance by integrating HIIT into their
training regimens. However, the mechanisms for these improvements
appear to differ.13 The rapid increases in skeletal muscle oxidative
enzymes seen in previously untrained exercisers are not apparent in
already trained individuals who add HIIT to their workouts. The
underlying adaptations for improved performance in these athletes
are not well understood.
Specificity of Training and Cross-Training
Physiological adaptations in response to physical training are highly
specific to the nature of the training activity. Furthermore, the more
specific the training program is to a given sport or activity, the greater
the improvement in performance in that sport or activity. As discussed
in chapter 9, the concept of specificity of training is very important
for all physiological adaptations.
This concept is also important in testing of athletes. As an
example, to accurately measure endurance improvements, athletes
should be tested while engaged in an activity similar to the sport or
activity in which they usually participate. Consider one study of highly
trained rowers, cyclists, and cross-country skiers. Their O2max was
measured while they performed two types of work: uphill running on a
treadmill and maximal performance of their sport-specific activity.33 A
key finding, shown in figure 11.20, was that the O2max attained by all
the athletes during their sport-specific activity was as high as or
higher than the values obtained on the treadmill. For many of these
athletes, O2max was substantially higher during their sport-specific
activity.
A highly creative design for studying the concept of specificity of
training involves one-legged exercise training, with the untrained
opposite leg used as the control. In one study, subjects were placed
into three groups: a group that sprint trained one leg and endurance
trained the other, a group that sprint trained one leg and did not train
the other, and a group that endurance trained one leg and did not
648
train the other.30 Improvement in O2max and lowered heart rate and
blood lactate response at submaximal work rates were found only
when exercise was performed with the endurance-trained leg.
FIGURE 11.20
O2max values measured during uphill treadmill running versus sport-specific activities
in selected groups of athletes.
Adapted by permission from S.B. Strømme, F. Ingjer, and H.D. Meen, “Assessment of Maximal Aerobic Power in
Specifically Trained Athletes,” Journal of Applied Physiology 42 (1977): 833-837.
Much of the training response occurs in the specific muscles that
have been trained, possibly even in individual motor units in a specific
muscle. This observation applies to metabolic as well as
cardiorespiratory responses to training. Table 11.5 shows the
activities of selected muscle enzymes from the three energy systems
649
for untrained, anaerobically trained, and aerobically trained men. The
table shows that aerobically trained muscles have significantly lower
glycolytic enzyme activities. Thus, they might have less capacity for
anaerobic metabolism or might rely less on energy from glycolysis.
More research is needed to explain the implications of the muscular
changes accompanying both anaerobic and aerobic training, but this
table clearly illustrates the high degree of specificity to a given
training stimulus.
Cross-training refers to training for more than one sport at the
same time or training several different fitness components (such as
endurance, strength, and flexibility) at one time. The athlete who
trains by swimming, running, and cycling in preparation for competing
in a triathlon is an example of the former, and the athlete involved in
heavy resistance training and high-intensity cardiorespiratory training
at the same time is an example of the latter.
TABLE 11.5 Selected Muscle Enzyme Activities (mmol · g−1 ·
min−1) for Untrained, Anaerobically Trained, and Aerobically
Trained Men
Untrained
Anaerobically trained
Aerobically trained
Aerobic enzymes
Oxidative system
Succinate dehydrogenase
Malate dehydrogenase
Carnitine palmityl transferase
8.1
45.5
1.5
8.0
46.0
1.5
20.8a
65.5a
2.3a
Anaerobic enzymes
ATP-PCr system
Creatine kinase
Myokinase
Glycolytic system
Phosphorylase
Phosphofructokinase
Lactate dehydrogenase
aSignificant
609.0
309.0
702.0a
350.0a
589.0
297.0
5.3
19.9
766.0
5.8
29.2a
811.0
3.7a
18.9
621.0
difference from the untrained value.
RESEARCH PERSPECTIVE 11.4
Age and Responses to HIIT
Maximal oxygen consumption ( O2max) is one of the strongest predictors of
cardiovascular health span and mortality. Even with regular aerobic activity,
O2max declines ~1% per year with age, and this decline accelerates in older
age. Consequently, older adults, who already have a higher risk for
cardiovascular disease and mortality, could benefit the most from interventions
650
that increase O2max. High-intensity interval training (HIIT) yields effective
improvements in aerobic fitness and cardiovascular heath in healthy young
and middle-aged adults. Because of the relatively short time commitment and
significant improvements in fitness achieved, HIIT may be an especially
valuable strategy for improving O2max in older adults. However, few research
studies have examined how age affects the aerobic training response to HIIT
in older adults.
A recent study of 94 healthy men and women ranging from 20 to 83 years
of age sought to determine how age affected improvements in
O2max
32
following HIIT training. In this study, participants with similar pretest O2max
values relative to age were tested immediately before and immediately
following an 8-week HIIT intervention. During the intervention, the study
participants completed supervised HIIT training with a targeted intensity of
90% to 95% of maximal heart rate, three times a week. After the HIIT
intervention, all of the subjects improved their O2max. In order to examine age
differences, the subjects were separated into six age groups (20-29 years, 3039 years, 40-49 years, 50-59 years, 60-69 years, and 70+ years). All of the
groups improved their O2max with no differences between age groups. In
contrast to age, the percentage improvements in O2max were predicted by
their baseline
O2max, with the least fit people showing the greatest
improvements regardless of their age group. Healthy individuals of average
fitness can improve O2max through HIIT, regardless of their age, and HIIT
may be a useful strategy to improve fitness and slow the decline in O2max in
healthy aging.
For the athlete training for cardiorespiratory endurance and
strength at the same time, the studies conducted to date indicate that
gains in strength, power, and endurance can result. However, the
gains in muscular strength and power are less when strength training
is combined with endurance training than when strength training
alone is done. The opposite does not appear to be true: Improvement
of aerobic power with endurance training does not appear to be
attenuated by inclusion of a resistance training program. In fact,
short-term endurance can be increased with resistance training.
Although earlier studies supported the conclusion that concurrent
strength and endurance training limits gains in strength and power,
McCarthy and colleagues23 reported similar gains in strength, muscle
hypertrophy, and neural activation in a group of previously untrained
subjects who underwent concurrent high-intensity strength training
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and cycle endurance training compared with a group who performed
only high-intensity strength training.
In Review
For athletes to maximize cardiorespiratory gains from training, the training should
be specific to the type of activity that an athlete usually performs.
The program must be carefully matched with the athlete’s individual needs to
maximize the physiological adaptations to training, thereby optimizing
performance.
Resistance training in combination with endurance training does not appear to
restrict improvement in aerobic power and may increase short-term endurance,
but it can limit improvement in strength and power when compared with gains
from resistance training alone.
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IN CLOSING
In this chapter, we examined how the cardiovascular, respiratory, and metabolic
systems adapt to aerobic and anaerobic training, as well as HIIT training. The
focus was on how these adaptations can improve both aerobic and anaerobic
performance. This chapter concludes our review of how body systems respond
to both acute and chronic exercise. Now that we have completed our
examination of how the body responds to internal challenges induced by various
types, durations, and intensities of exercise, we turn our attention to the external
environment. In the next part of the book, we focus on the body’s adaptations to
varying environmental conditions, beginning in the next chapter by considering
how external temperature can affect performance.
KEY TERMS
aerobic training
anaerobic training
athlete’s heart
capillary-to-fiber ratio
cardiac hypertrophy
cross-training
Fick equation
glycogen sparing
high responders
low responders
mitochondrial oxidative enzymes
oxygen transport system
specificity of training
submaximal endurance
STUDY QUESTIONS
1.
2.
Differentiate between muscular endurance and cardiovascular endurance.
3.
Of what importance is O2max to endurance performance? Why does the
competitor with the highest O2max not always win?
4.
Describe the changes in the oxygen transport system that occur with
endurance training.
5.
What is possibly the most important adaptation that the body makes in
response to endurance training, which allows for an increase in both
What is maximal oxygen uptake ( O2max)? How is it defined physiologically,
and what determines its limits?
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O2max and performance? Through what mechanisms do these changes
occur?
6.
What are the theoretical reasons given for the resting bradycardia that
accompanies endurance exercise training?
7.
8.
What metabolic adaptations occur in response to endurance training?
9.
What is the most important predictor of how much
inactivity or bed rest?
Explain the two theories that have been proposed to account for limitations
to aerobic performance that may be altered by endurance training. Which of
these has the greatest validity today?
O2max will decline with
10.
11.
How important is genetic potential in a developing young athlete?
12.
Discuss specificity of anaerobic training with respect to enzyme changes in
muscle.
13.
Can athletes who already train vigorously still improve performance by
integrating HIIT into their training regimens? In what way are adaptive
mechanisms different from those seen in untrained individuals who undergo
HIIT?
14.
Why is cross-training beneficial to endurance athletes? How does it benefit
sprint and power athletes?
What adaptations have been shown to occur in muscle fibers with
anaerobic training?
STUDY GUIDE ACTIVITIES
In addition to the activities listed in the chapter opening outline, two other
activities are available in the web study guide, located at
www.HumanKinetics.com/PhysiologyOfSportAndExercise
The KEY TERMS activity reviews important terms, and the end-of-chapter QUIZ
tests your understanding of the material covered in the chapter.
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PART IV
Environmental Influences on
Performance
In previous sections of this book, we discussed the physiological
adjustments and coordination of systems (muscular, neural,
cardiovascular, respiratory) that allow us to perform physical activity.
We also saw how these systems adapt when exposed to the
repeated stress of training. In part IV, we turn our attention to how
the body responds and adapts when challenged to exercise under
extreme environmental conditions. In chapter 12, Exercise in Hot
and Cold Environments, we examine the mechanisms by which the
body regulates its internal temperature at rest and during exercise.
Then we consider how the body responds and adapts to exercise in
the heat and cold, along with the health risks associated with
physical activity in hot and cold environments. In chapter 13,
Exercise at Altitude, we discuss the unique challenges that the body
faces when performing physical activity under conditions of reduced
atmospheric pressure (altitude) and how the body adapts to time
spent at altitude. We then discuss the best way to prepare for
competing at altitude and whether altitude training might help people
perform better at sea level. Finally, health risks associated with
ascent to high altitude are discussed.
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12
Exercise in Hot and Cold Environments
In this chapter and in the web study guide
Body Temperature Regulation
Metabolic Heat Production
Transfer of Body Heat to and From the Environment
Thermoregulatory Control
ANIMATION FOR FIGURE 12.5 shows the hypothalamus’ response to changes in
body temperature.
ACTIVITY 12.1 Control of Heat Exchange explores the role of the hypothalamus in
controlling body temperature.
Physiological Responses to Exercise in the Heat
Cardiovascular Function
What Limits Exercise in the Heat?
Body Fluid Balance: Sweating
VIDEO 12.1 presents Caroline Smith on research methods for measuring sweat
rates over different parts of the body and the findings of this research.
ACTIVITY 12.2 Exercise in the Heat reviews changes in physiological responses
due to exercising in the heat.
Health Risks During Exercise in the Heat
Measuring Heat Stress
Heat-Related Disorders
Sickle Cell Trait Complications
Preventing Hyperthermia
ACTIVITY 12.3 Heat-Related Disorders investigates three athlete scenarios
covering the signs, symptoms, and treatment of heat cramps, heat exhaustion,
and heatstroke.
Acclimation to Exercise in the Heat
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Effects of Heat Acclimation
Achieving Heat Acclimation
Sex Differences
Exercise in the Cold
Habituation and Acclimation to Cold
Other Factors Affecting Body Heat Loss
Heat Loss in Cold Water
Physiological Responses to Exercise in the Cold
Muscle Function
Metabolic Responses
ACTIVITY 12.4 Exercise in the Cold reviews changes in physiological responses
due to exercising in the cold.
Health Risks During Exercise in the Cold
Hypothermia
Cardiorespiratory Effects
Frostbite
Exercise-Induced Asthma
ANIMATION FOR FIGURE 12.15 shows the warming of air as it enters the
respiratory system.
ACTIVITY 12.5 Cold-Related Health Risks investigates two recreational scenarios
covering the signs, symptoms, and treatment of health risks related to exercising
in the cold.
In Closing
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O
rganizers of the 2014 Australian (Tennis) Open were criticized for forcing
players to compete in intense heat as temperatures hit 42 °C (108 °F) in Melbourne
on January 13. The day’s peak temperature of 42 °C was just short of Melbourne’s
January record of 45.6 °C (114 °F), which occurred in 1936. The Olympic
Movement Medical Code states, “In each sports discipline, minimal safety
requirements should be defined and applied with a view to protecting the health of
the participants and the public during training and competition. Depending on the
sport and the level of competition, specific rules should be adopted regarding
sports venues [and] safe environmental conditions.”5 All major sporting bodies
abide by this code and have comprehensive management strategies in place.
However, the Australian Open Extreme Heat Policy (EHP) is applied only at the
referee’s discretion, and only minimal changes were enacted to protect the players
in Melbourne.
Several prominent competitors, including Scotland’s Andy Murray,
unsuccessfully called on Australian Open organizers to reconsider their decision to
make players compete in such oppressive temperatures. Canadian player Frank
Dancevic passed out during the second set of his first-round match with France’s
Benoit Paire on an unshaded court, as did a ball boy. It was so hot that Danish
player Caroline Wozniacki’s plastic water bottle melted on court and Serbia’s
Jelena Jankovic burned her backside and hamstrings sitting on an uncovered seat,
then fell during her first-round victory when her rubber-soled shoe stuck to the
court. Yet play continued.
The stresses of physical exertion are often complicated by
environmental conditions. Performing exercise in extreme heat or
cold places an additional burden on the mechanisms that regulate
body temperature while supporting continued exercise. Although
these mechanisms are amazingly effective in regulating body
temperature
under
normal
conditions,
mechanisms
of
thermoregulation can be inadequate when we are subjected to
extreme heat or cold. Fortunately, the body is able to adapt to such
environmental stresses with continued exposure over time, a
process known as acclimation (which refers to a short-term
adaptation, e.g., days to weeks) or acclimatization (the proper term
when we are referring to natural adaptations gained over long
periods of time, e.g., months to years).
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In the following discussion, we focus on the physiological
responses to acute and chronic exercise in both hot and cold
environments. Specific health risks are associated with exercise in
both temperature extremes, so we also discuss the prevention of
temperature-related illness and injuries during exercise.
Body Temperature Regulation
Humans are homeotherms, which means that our internal body
temperature is physiologically regulated to keep it nearly constant
even when environmental temperature changes. In physiology,
temperatures are expressed as degrees Centigrade. To convert from
°F to °C and vice versa, use the following transformations:
To go from °F to °C: Subtract 32°, then divide by 1.8.
To go from °C to °F: Multiply by 1.8, then add 32°.
Although a person’s temperature varies from day to day, and even
from hour to hour, these fluctuations are usually no more than about
1.0 °C (1.8 °F). Only during prolonged heavy exercise, fever due to
illness, or extreme conditions of heat or cold do body temperatures
deviate from the normal baseline range of 36.1 to 37.8 °C (97.0100.0 °F). Body temperature reflects a careful balance between heat
production and heat loss. Whenever this balance is disturbed, body
temperature changes.
Metabolic Heat Production
Only a small part (usually less than 25%) of the energy (adenosine
triphosphate, ATP) the body produces is used for physiological
functions such as muscle contraction; the rest is converted to heat.
All active tissues produce metab